automated-analytics/bionlp2004 · Datasets at AI快站

400

Neither DNA fragmentation nor the morphology of apoptosis was observed .

401

These findings demonstrate that cross-linking of MHC class II molecules transduced the negative signals through intracellular mechanisms different from those present in the cross-linking of surface IgM .

These findings demonstrate that cross-linking of <protein>MHC class II molecules</protein> transduced the negative signals through intracellular mechanisms different from those present in the cross-linking of surface <protein>IgM</protein> .

402

Functional block for 1 alpha , 25-dihydroxyvitamin D3-mediated gene regulation in human B lymphocytes .

Functional block for 1 alpha , 25-dihydroxyvitamin D3-mediated gene regulation in <cell_type>human B lymphocytes</cell_type> .

403

Elements necessary for the steroid hormone 1 alpha , 25-dihydroxyvitamin D3 ( 1 alpha , 25- ( OH ) 2D3 ) to induce a biological response include the presence of specific intracellular receptors ( vitamin D3 receptors ( VDR ) ) and modulation of gene expression via hormone-activated receptor binding to regulatory regions of target genes .

Elements necessary for the steroid hormone 1 alpha , 25-dihydroxyvitamin D3 ( 1 alpha , 25- ( OH ) 2D3 ) to induce a biological response include the presence of specific <protein>intracellular receptors</protein> ( <protein>vitamin D3 receptors</protein> ( <protein>VDR</protein> ) ) and modulation of gene expression via hormone-activated receptor binding to <protein>regulatory regions</protein> of <dna>target genes</dna> .

404

These parameters were examined in normal and Epstein-Barr virus-immortalized human B cells and compared with 1 alpha , 25- ( OH ) 2D3-responsive cells of the T and monocytic lineages .

These parameters were examined in normal and <cell_line>Epstein-Barr virus-immortalized human B cells</cell_line> and compared with <cell_line>1 alpha , 25- ( OH ) 2D3-responsive cells</cell_line> of the <cell_type>T and monocytic lineages</cell_type> .

405

Although resting tonsillar B cells did not express VDR mRNA , activation of these cells with interleukin-4 induced VDR in the absence of exogenously supplemented 1 alpha , 25- ( OH ) 2D3 .

Although resting tonsillar B cells did not express <rna>VDR mRNA</rna> , activation of these cells with <protein>interleukin-4</protein> induced <protein>VDR</protein> in the absence of exogenously supplemented 1 alpha , 25- ( OH ) 2D3 .

406

As indicators of hormone-mediated gene regulation we analyzed modulation of CD23 , a common B cell/monocyte surface antigen , and 24-hydroxylase .

As indicators of hormone-mediated gene regulation we analyzed modulation of <protein>CD23</protein> , a <protein>common B cell/monocyte surface antigen</protein> , and <protein>24-hydroxylase</protein> .

407

1 alpha , 25- ( OH ) 2D3 inhibited CD23 expression in U937 cells , yet failed to modulate CD23 expression in B cells .

1 alpha , 25- ( OH ) 2D3 inhibited <protein>CD23</protein> expression in <cell_line>U937 cells</cell_line> , yet failed to modulate <protein>CD23</protein> expression in <cell_type>B cells</cell_type> .

408

Furthermore , 1 alpha , 25- ( OH ) 2D3 induced 24-hydroxylase mRNA expression and metabolic activity in both U937 cells and lectin-activated T cells , yet failed to induce 24-hydroxylase mRNA or its metabolic activity in B cells .

Furthermore , 1 alpha , 25- ( OH ) 2D3 induced <protein>24-hydroxylase</protein> mRNA expression and metabolic activity in both <cell_line>U937 cells</cell_line> and <cell_type>lectin-activated T cells</cell_type> , yet failed to induce <rna>24-hydroxylase mRNA</rna> or its metabolic activity in <cell_type>B cells</cell_type> .

409

These findings suggest that although human B lymphocytes can express VDR mRNA and protein , they exhibit a functional block for vitamin D-dependent gene regulation .

These findings suggest that although <cell_type>human B lymphocytes</cell_type> can express <rna>VDR mRNA</rna> and <protein>protein</protein> , they exhibit a functional block for vitamin D-dependent gene regulation .

410

Positive and negative regulation of IL-2 gene expression : role of multiple regulatory sites .

Positive and negative regulation of <protein>IL-2</protein> gene expression : role of multiple regulatory sites .

411

Interleukin 2 ( IL-2 ) is an important lymphokine required in the process of T cell activation , proliferation , clonal expansion and differentiation .

Interleukin 2 ( <protein>IL-2</protein> ) is an important <protein>lymphokine</protein> required in the process of T cell activation , proliferation , clonal expansion and differentiation .

412

The IL-2 gene displays both T cell specific and inducible expression : it is only expressed in CD4+ T cells after antigenic or mitogenic stimulation .

The <dna>IL-2 gene</dna> displays both T cell specific and inducible expression : it is only expressed in <cell_type>CD4+ T cells</cell_type> after antigenic or mitogenic stimulation .

413

Several cis-acting regulatory sites are required for induction of the IL-2 gene after stimulation .

Several <dna>cis-acting regulatory sites</dna> are required for induction of the <dna>IL-2 gene</dna> after stimulation .

414

In this study , we have analysed the function of these cis-acting regulatory sites in the context of the native IL-2 enhancer and promoter sequence .

In this study , we have analysed the function of these <dna>cis-acting regulatory sites</dna> in the context of the native <dna>IL-2 enhancer</dna> and <dna>promoter sequence</dna> .

415

The results of this study suggest that the NFAT ( -276 to -261 ) , the distal octamer ( -256 to -248 ) and the proximal octamer ( -75 to -66 ) sites not only act as enhancers of IL-2 gene transcription in the presence of cellular stimulation , but also have a silencing effect on IL-2 gene expression in resting cells .

The results of this study suggest that the <protein>NFAT</protein> ( <dna>-276 to -261</dna> ) , the <dna>distal octamer</dna> ( <dna>-256 to -248</dna> ) and the <dna>proximal octamer</dna> ( <dna>-75 to -66</dna> ) sites not only act as enhancers of <dna>IL-2 gene</dna> transcription in the presence of cellular stimulation , but also have a silencing effect on <dna>IL-2 gene</dna> expression in resting cells .

416

Two other sites display disparate effects on IL-2 gene expression in different T leukemia cell lines : the distal purine box ( -291 to -277 ) and the proximal purine box sites ( -145 to -128 ) .

Two other sites display disparate effects on <dna>IL-2 gene</dna> expression in different <cell_line>T leukemia cell lines</cell_line> : the <dna>distal purine box</dna> ( <dna>-291 to -277</dna> ) and the <dna>proximal purine box sites</dna> ( <dna>-145 to -128</dna> ) .

417

Finally , the AP-1 ( -186 to -176 ) and the kappa B sites ( -206 to -195 ) respond to different cellular activation in EL4 cells .

Finally , the <dna>AP-1 ( -186 to -176 ) and the kappa B sites</dna> ( <dna>-206 to -195</dna> ) respond to different cellular activation in <cell_line>EL4 cells</cell_line> .

418

The AP-1 site mediated the response to PMA stimulation while the kappa B site responded to IL-1 stimulation .

The <dna>AP-1 site</dna> mediated the response to PMA stimulation while the <dna>kappa B site</dna> responded to <protein>IL-1</protein> stimulation .

419

These data suggest that the regulation of IL-2 gene expression is a complex process and multiple cis-acting regulatory sites interact to exert different effects in T cells representative of alternative stages of differentiation .

These data suggest that the regulation of <dna>IL-2 gene</dna> expression is a complex process and multiple <dna>cis-acting regulatory sites</dna> interact to exert different effects in <cell_type>T cells</cell_type> representative of alternative stages of differentiation .

420

Sp1 is a critical factor for the monocytic specific expression of human CD14 .

<protein>Sp1</protein> is a critical factor for the monocytic specific expression of <protein>human CD14</protein> .

421

CD14 is a membrane glycoprotein expressed specifically on monocytes and macrophages , and its expression is markedly increased during the process of monocyte differentiation .

<protein>CD14</protein> is a <protein>membrane glycoprotein</protein> expressed specifically on <cell_type>monocytes</cell_type> and <cell_type>macrophages</cell_type> , and its expression is markedly increased during the process of <cell_type>monocyte</cell_type> differentiation .

422

In order to study CD14 gene regulation , the human CD14 gene was cloned from a partial EcoRI digested chromosome 5 library .

In order to study <dna>CD14 gene</dna> regulation , the <dna>human CD14 gene</dna> was cloned from a partial <dna>EcoRI digested chromosome 5 library</dna> .

423

A 5.5-kilobase genomic clone contained the full-length CD14 coding sequence and 4.2 kilobases of 5'-upstream sequence .

A <dna>5.5-kilobase genomic clone</dna> contained the full-length <dna>CD14 coding sequence</dna> and <dna>4.2 kilobases of 5'-upstream sequence</dna> .

424

One major and one minor transcription start site were identified 101 and 130 base pairs ( bp ) upstream , respectively , from the protein translation start ATG .

One <dna>major and one minor transcription start site</dna> were identified <dna>101 and 130 base pairs ( bp ) upstream</dna> , respectively , from the <dna>protein translation start ATG</dna> .

425

A DNA fragment containing 128 bp of upstream sequence had strong , monocyte-specific promoter activity in the CD14 positive monocytic cell line Mono Mac 6 as compared to the nonmonocytic cell lines HeLa and REX .

A <dna>DNA fragment</dna> containing <dna>128 bp of upstream sequence</dna> had strong , monocyte-specific promoter activity in the <cell_line>CD14 positive monocytic cell line</cell_line> <cell_line>Mono Mac 6</cell_line> as compared to the <cell_line>nonmonocytic cell lines</cell_line> <cell_line>HeLa</cell_line> and <cell_line>REX</cell_line> .

426

Four regions in this DNA fragment interact with nuclear proteins isolated from monocytic cells .

Four regions in this <dna>DNA fragment</dna> interact with <protein>nuclear proteins</protein> isolated from <cell_type>monocytic cells</cell_type> .

427

The Sp1 transcription factor bound to three different regions in the CD14 promoter .

The <protein>Sp1</protein> <protein>transcription factor</protein> bound to three different regions in the <dna>CD14 promoter</dna> .

428

Mutation of the major Sp1 binding site ( -110 bp ) decreased tissue-specific promoter activity , and these results , together with transactivation experiments , demonstrate that Sp1 plays a critical role in the tissue-specific expression of CD14 in monocytic cells .

Mutation of the <dna>major Sp1 binding site</dna> ( <dna>-110 bp</dna> ) decreased tissue-specific promoter activity , and these results , together with transactivation experiments , demonstrate that <protein>Sp1</protein> plays a critical role in the tissue-specific expression of <protein>CD14</protein> in <cell_type>monocytic cells</cell_type> .

429

CD14 Sp1 site oligonucleotides bound preferentially to a 105-kDa Sp1 species , which is present in higher relative levels in monocytic than non-monocytic cells , suggesting that modification of Sp1 , such as phosphorylation , may explain how the Sp1 site mediates monocytic specific promoter activity .

<protein>CD14</protein> <protein>Sp1</protein> site oligonucleotides bound preferentially to a <protein>105-kDa Sp1 species</protein> , which is present in higher relative levels in <cell_type>monocytic</cell_type> than <cell_type>non-monocytic cells</cell_type> , suggesting that modification of <protein>Sp1</protein> , such as phosphorylation , may explain how the <protein>Sp1</protein> site mediates monocytic specific promoter activity .

430

The interleukin-8 AP-1 and kappa B-like sites are genetic end targets of FK506-sensitive pathway accompanied by calcium mobilization .

The <dna>interleukin-8 AP-1 and kappa B-like sites</dna> are genetic end targets of FK506-sensitive pathway accompanied by calcium mobilization .

431

FK506 , an immunosuppressant , inhibits the production of several cytokines in T lymphocytes .

FK506 , an immunosuppressant , inhibits the production of several <protein>cytokines</protein> in <cell_type>T lymphocytes</cell_type> .

432

We observed that FK506 suppressed the transcription of a chemotactic cytokine , interleukin-8 ( IL-8 ) in a human T cell line , Jurkat cells , activated by phorbol 12-myristate 13-acetate ( PMA ) and calcium ( Ca2+ ) ionophore ( ionomycin ) .

We observed that FK506 suppressed the transcription of a <protein>chemotactic cytokine</protein> , <protein>interleukin-8</protein> ( <protein>IL-8</protein> ) in a <cell_line>human T cell line</cell_line> , <cell_line>Jurkat cells</cell_line> , activated by phorbol 12-myristate 13-acetate ( PMA ) and calcium ( Ca2+ ) ionophore ( ionomycin ) .

433

By deleted and mutated analysis of the IL-8 promoters , the AP-1 and kappa B-like sites were identified as the responsive elements for PMA and ionomycin .

By deleted and mutated analysis of the <dna>IL-8 promoters</dna> , the <dna>AP-1 and kappa B-like sites</dna> were identified as the responsive elements for PMA and ionomycin .

434

FK506 suppressed the transcriptions through the AP-1 or kappa B-like sites induced by PMA plus Ca ( 2+ ) -mobilizing agents , but not those induced by Ca ( 2+ ) -independent stimuli .

FK506 suppressed the transcriptions through the <dna>AP-1</dna> or <dna>kappa B-like sites</dna> induced by PMA plus Ca ( 2+ ) -mobilizing agents , but not those induced by Ca ( 2+ ) -independent stimuli .

435

In gel retardation analysis , FK506 had little effect on the binding to the AP-1 site of PMA/ionomycin-induced nuclear factors , which were recognized with anti-JunD or c-Fos antibody .

In gel retardation analysis , FK506 had little effect on the binding to the <dna>AP-1 site</dna> of PMA/ionomycin-induced nuclear factors , which were recognized with <protein>anti-JunD</protein> or <protein>c-Fos antibody</protein> .

436

In contrast , FK506 or EGTA ( Ca2+ chelator ) similarly affected the formation of kappa B-like site binding complexes , which were not recognized by any antibodies against the human Rel family proteins ( c-Rel , p65 , p50 , and p49 ) .

In contrast , FK506 or EGTA ( Ca2+ chelator ) similarly affected the formation of <protein>kappa B-like site binding complexes</protein> , which were not recognized by any <protein>antibodies</protein> against the <protein>human Rel family proteins</protein> ( <protein>c-Rel</protein> , <protein>p65</protein> , <protein>p50</protein> , and <protein>p49</protein> ) .

437

Furthermore , we confirmed the previous report that FK506 suppressed the PMA/ionomycin-induced activation through authentic kappa B site of immunoglobulin ( Ig ) gene , to which NF-kappa B binding was also decreased by FK506 , indicating that both IL-8 kappa B-like site and Ig kappa B site are FK506-sensitive in spite of the difference of binding factors .

Furthermore , we confirmed the previous report that FK506 suppressed the PMA/ionomycin-induced activation through authentic <dna>kappa B site</dna> of <dna>immunoglobulin ( Ig ) gene</dna> , to which <protein>NF-kappa B</protein> binding was also decreased by FK506 , indicating that both <dna>IL-8 kappa B-like site</dna> and Ig <dna>kappa B site</dna> are FK506-sensitive in spite of the difference of <protein>binding factors</protein> .

438

Our results indicate that not only the reported IL-2 NF-AT and NFIL-2A sites and Ig kappa B site , but also the IL-8 AP-1 and kappa B-like sites are terminals of FK506-sensitive pathway involving Ca2+ mobilization .

Our results indicate that not only the reported <dna>IL-2 NF-AT and NFIL-2A sites</dna> and Ig <dna>kappa B site</dna> , but also the <protein>IL-8</protein> <dna>AP-1</dna> and <dna>kappa B-like sites</dna> are terminals of FK506-sensitive pathway involving Ca2+ mobilization .

439

Androgen binding sites in peripheral human mononuclear leukocytes of healthy males and females .

<protein>Androgen binding sites</protein> in <cell_type>peripheral human mononuclear leukocytes</cell_type> of healthy males and females .

440

Androgen binding sites have been identified in circulating human mononuclear leukocytes of healthy donors of both sexes .

<protein>Androgen binding sites</protein> have been identified in <cell_type>circulating human mononuclear leukocytes</cell_type> of healthy donors of both sexes .

441

Cells were separated from blood samples on a Ficoll gradient and incubated with different concentrations of [ 3H ] testosterone in the presence or absence of a 400-fold excess of unlabelled testosterone .

442

Binding data were derived from Scatchard analysis .

443

The binding sites fulfil the required criteria for specific steroid binding sites however differ somewhat from the classic androgen receptors from genital skin fibroblast : in fertile adult males ( n = 20 ) the binding sites showed ( 1 ) a high affinity for testosterone ( 1.32 +/- 0.49 nM ; mean +/- SD ) , ( 2 ) a saturable capacity ( 184 +/- 52 binding sites per cell ; mean +/- SD ) , and ( 3 ) a characteristic competitive binding profile for other steroid hormones ( relative binding affinities : testosterone = dihydrotestosterone > 17 beta-estradiol > progesterone , whereas aldosterone , 17-hydroxy-progesterone and cortisol did not compete appreciably ) .

The <protein>binding sites</protein> fulfil the required criteria for specific <protein>steroid binding sites</protein> however differ somewhat from the classic <protein>androgen receptors</protein> from <cell_type>genital skin fibroblast</cell_type> : in fertile adult males ( n = 20 ) the <protein>binding sites</protein> showed ( 1 ) a high affinity for testosterone ( 1.32 +/- 0.49 nM ; mean +/- SD ) , ( 2 ) a saturable capacity ( 184 +/- 52 <protein>binding sites</protein> per cell ; mean +/- SD ) , and ( 3 ) a characteristic competitive binding profile for other steroid hormones ( relative binding affinities : testosterone = dihydrotestosterone > 17 beta-estradiol > progesterone , whereas aldosterone , 17-hydroxy-progesterone and cortisol did not compete appreciably ) .

444

Furthermore the number of binding sites determined using [ 3H ] dihydrotestosterone , [ 3H ] RU-1881 , or [ 3H ] testosterone were comparable .

Furthermore the number of <protein>binding sites</protein> determined using [ 3H ] dihydrotestosterone , [ 3H ] RU-1881 , or [ 3H ] testosterone were comparable .

445

This raises the possibility that androgen receptors in peripheral mononuclear leukocytes differ from those in genital skin fibroblasts .

This raises the possibility that <protein>androgen receptors</protein> in <cell_type>peripheral mononuclear leukocytes</cell_type> differ from those in <cell_type>genital skin fibroblasts</cell_type> .

446

There was no apparent correlation between serum testosterone concentrations and androgen binding sites .

There was no apparent correlation between serum testosterone concentrations and <protein>androgen binding sites</protein> .

447

In fertile women remarkable changes in androgen binding sites were seen in the course of the menstrual cycle , with a significant increase in the immediate preovulatory period .

In fertile women remarkable changes in <protein>androgen binding sites</protein> were seen in the course of the menstrual cycle , with a significant increase in the immediate preovulatory period .

448

The presence of androgen receptors in peripheral mononuclear leukocytes provides for the first time the experimental basis for an hypothesis of direct , receptor-mediated effects of androgens on mature immunocompetent cells .

The presence of <protein>androgen receptors</protein> in <cell_type>peripheral mononuclear leukocytes</cell_type> provides for the first time the experimental basis for an hypothesis of direct , receptor-mediated effects of androgens on <cell_type>mature immunocompetent cells</cell_type> .

449

The immunological implications of these results are discussed .

450

Induction of IL-8 expression in T cells uses the CD28 costimulatory pathway .

Induction of <protein>IL-8</protein> expression in <cell_type>T cells</cell_type> uses the <protein>CD28</protein> costimulatory pathway .

451

IL-8 , a potent chemotactic factor for neutrophil granulocytes and lymphocytes , is a proinflammatory cytokine secreted by a variety of cell types , including T cells .

<protein>IL-8</protein> , a potent <protein>chemotactic factor</protein> for <cell_type>neutrophil granulocytes</cell_type> and <cell_type>lymphocytes</cell_type> , is a proinflammatory cytokine secreted by a variety of cell types , including <cell_type>T cells</cell_type> .

452

Stimulation of the CD28 cell surface molecule delivers costimulatory signals essential for lymphokine production in activated T cells via a conserved sequence element found in the promoter of several lymphokine genes .

Stimulation of the <protein>CD28 cell surface molecule</protein> delivers costimulatory signals essential for <protein>lymphokine</protein> production in <cell_type>activated T cells</cell_type> via a <dna>conserved sequence element</dna> found in the <dna>promoter</dna> of several <dna>lymphokine genes</dna> .

453

Anti-CD28-stimulated T cells produced significant amounts of IL-8 ; additionally , costimulation with anti-CD3 and anti-CD28 Abs resulted in a synergistic induction of IL-8 secretion .

<cell_line>Anti-CD28-stimulated T cells</cell_line> produced significant amounts of <protein>IL-8</protein> ; additionally , costimulation with <protein>anti-CD3</protein> and <protein>anti-CD28 Abs</protein> resulted in a synergistic induction of <protein>IL-8</protein> secretion .

454

Sequence homology , single nucleotide mutations , and anti-CD28 Ab stimulation studies established that the NF-kappa B-like sequence in the promoter of the IL-8 gene functioned as a CD28 response element .

Sequence homology , single nucleotide mutations , and <protein>anti-CD28 Ab</protein> stimulation studies established that the <dna>NF-kappa B-like sequence</dna> in the <dna>promoter</dna> of the <dna>IL-8 gene</dna> functioned as a <dna>CD28 response element</dna> .

455

Furthermore , cyclosporin A , but not rapamycin , blocked the synergistic induction of IL-8 expression achieved with anti-CD3 and anti- CD28 costimulation .

Furthermore , cyclosporin A , but not rapamycin , blocked the synergistic induction of <protein>IL-8</protein> expression achieved with <protein>anti-CD3</protein> and anti- <protein>CD28</protein> costimulation .

456

The involvement of a CD28 response element in the induction of IL-8 expression in activated T cells may provide new insights into the pathogenesis and persistence of immune disorders characterized by increased levels of IL-8 , such as psoriasis and rheumatoid arthritis .

The involvement of a <dna>CD28 response element</dna> in the induction of <protein>IL-8</protein> expression in <cell_type>activated T cells</cell_type> may provide new insights into the pathogenesis and persistence of immune disorders characterized by increased levels of <protein>IL-8</protein> , such as psoriasis and rheumatoid arthritis .

457

MHC class II signaling in B-cell activation [ see comments ]

<protein>MHC class II</protein> signaling in <cell_type>B-cell</cell_type> activation [ see comments ]

458

The cognate interaction between T cells and antigen-presenting cells ( APCs ) , mediated by major histocompatibility complex ( MHC ) class II molecules , results in the delivery of activation signals to the APC .

The cognate interaction between <cell_type>T cells</cell_type> and <cell_type>antigen-presenting cells</cell_type> ( <cell_type>APCs</cell_type> ) , mediated by <protein>major histocompatibility complex ( MHC ) class II molecules</protein> , results in the delivery of activation signals to the <cell_type>APC</cell_type> .

459

These signals contribute to the expression of co-stimulatory activity by APCs and have important consequences for cell effector function .

These signals contribute to the expression of co-stimulatory activity by <cell_type>APCs</cell_type> and have important consequences for cell effector function .

460

MHC class II molecules also serve as receptors for B-cell stimulation by microbial superantigens .

<protein>MHC class II</protein> molecules also serve as receptors for <cell_type>B-cell</cell_type> stimulation by <protein>microbial superantigens</protein> .

461

In this review , Paul Scholl and Raif Geha discuss recent advances in our understanding of mechanisms of MHC class II signaling and analyse their role in human B-cell activation .

In this review , Paul Scholl and Raif Geha discuss recent advances in our understanding of mechanisms of <protein>MHC class II</protein> signaling and analyse their role in human <cell_type>B-cell</cell_type> activation .

462

Effects of glucocorticoids in rheumatoid arthritis .

463

Diminished glucocorticoid receptors do not result in glucocorticoid resistance .

Diminished <protein>glucocorticoid receptors</protein> do not result in glucocorticoid resistance .

464

OBJECTIVE .

465

Lymphocytes of patients with rheumatoid arthritis ( RA ) have diminished receptor density ; thus , patients with RA should show partial resistance to glucocorticoids .

466

We investigated the glucocorticoid sensitivity of lymphocytes in RA patients compared with healthy subjects .

We investigated the glucocorticoid sensitivity of <cell_type>lymphocytes</cell_type> in RA patients compared with healthy subjects .

467

METHODS .

468

We determined the effects of glucocorticoids on lymphocyte proliferation and cytokine release .

We determined the effects of glucocorticoids on <cell_type>lymphocyte</cell_type> proliferation and <protein>cytokine</protein> release .

469

RESULTS .

470

Proliferation and cytokine release were inhibited in RA patients to the same extent as in healthy controls .

Proliferation and <protein>cytokine</protein> release were inhibited in RA patients to the same extent as in healthy controls .

471

CONCLUSION .

472

Diminished receptor density in RA patients does not result in glucocorticoid resistance .

473

Arrested development : understanding v-abl .

Arrested development : understanding <dna>v-abl</dna> .

474

The protein tyrosine kinase activity of the v-abl oncogene has been demonstrated to subvert the normal second messenger systems used by lymphoid cells for growth and differentiation .

The <protein>protein tyrosine kinase</protein> activity of the <dna>v-abl oncogene</dna> has been demonstrated to subvert the normal second messenger systems used by <cell_type>lymphoid cells</cell_type> for growth and differentiation .

475

Transformation of bone marrow with the Abelson murine leukemia virus results in the appearance of B cell lineage cells arrested at the pre-B cell stage .

Transformation of bone marrow with the Abelson murine leukemia virus results in the appearance of <cell_type>B cell lineage cells</cell_type> arrested at the pre-B cell stage .

476

Recent reports have characterized these cells expressing high v-abl kinase activity as deficient in detectable NF-kappaB DNA binding activity and low level RAG gene expression .

Recent reports have characterized these cells expressing high <dna>v-abl</dna> kinase activity as deficient in detectable <protein>NF-kappaB</protein> DNA binding activity and low level <dna>RAG gene</dna> expression .

477

These observations suggest that v-abl may be inhibiting the differentiation of B cells by blocking these two crucial elements in the maturation pathway .

These observations suggest that <dna>v-abl</dna> may be inhibiting the differentiation of <cell_type>B cells</cell_type> by blocking these two crucial elements in the maturation pathway .

478

Corticosteroid receptors in lymphocytes : a possible marker of brain involution ?

<protein>Corticosteroid receptors</protein> in <cell_type>lymphocytes</cell_type> : a possible marker of brain involution ?

479

A similarity has recently been found between the regulation of corticosteroid receptors in brain and in lymphoid tissue .

A similarity has recently been found between the regulation of <protein>corticosteroid receptors</protein> in brain and in lymphoid tissue .

480

We have studied the regulation of corticosteroid receptors in human mononuclear leukocytes as a possible marker of brain involution .

We have studied the regulation of <protein>corticosteroid receptors</protein> in <cell_type>human mononuclear leukocytes</cell_type> as a possible marker of brain involution .

481

Type I corticosteroid receptors are down regulated by excess of mineralocorticoids ( primary and secondary hyperaldosteronism , pseudohyperaldosteronism ) and of glucocorticoids ( Cushing 's syndrome ) . Type II corticosteroid receptors are not reduced by excess of endogenous corticosteroids ( Cushing 's syndrome ) .

<protein>Type I corticosteroid receptors</protein> are down regulated by excess of mineralocorticoids ( primary and secondary hyperaldosteronism , pseudohyperaldosteronism ) and of glucocorticoids ( Cushing 's syndrome ) . <protein>Type II corticosteroid receptors</protein> are not reduced by excess of endogenous corticosteroids ( Cushing 's syndrome ) .

482

In normal adults there is a direct significant correlation between plasma cortisol and Type I and between plasma cortisol and Type II receptors in mononuclear leukocytes , while in Cushing 's syndrome the correlation is inverse between plasma cortisol at 8 a.m. and Type II receptors .

In normal adults there is a direct significant correlation between plasma cortisol and <protein>Type I</protein> and between plasma cortisol and <protein>Type II receptors</protein> in <cell_type>mononuclear leukocytes</cell_type> , while in Cushing 's syndrome the correlation is inverse between plasma cortisol at 8 a.m. and <protein>Type II receptors</protein> .

483

In an aged population the mean numbers of Type I and of Type II receptors are lower and plasma cortisol is higher than in adult controls , but the increase of plasma cortisol is not followed by a clinical picture of hypercorticism .

In an aged population the mean numbers of <protein>Type I</protein> and of <protein>Type II receptors</protein> are lower and plasma cortisol is higher than in adult controls , but the increase of plasma cortisol is not followed by a clinical picture of hypercorticism .

484

Corticosteroid Type I and Type II receptors are inversely correlated with age .

<protein>Corticosteroid Type I and Type II receptors</protein> are inversely correlated with age .

485

After dexamethasone suppression ( 1 mg at 11 p.m. ) Type I receptors always decrease in controls while the response of Type II is not homogeneous .

After dexamethasone suppression ( 1 mg at 11 p.m. ) <protein>Type I receptors</protein> always decrease in controls while the response of <protein>Type II</protein> is not homogeneous .

486

In an aged group of patients , both receptors are reduced by dexamethasone .

487

We conclude that the decrease with age of corticosteroid receptors is possibly related to a physiological involution of corticosteroid receptors and that this reduction does increase plasma cortisol concentration , without affecting the glucocorticoid effector mechanism .

We conclude that the decrease with age of <protein>corticosteroid receptors</protein> is possibly related to a physiological involution of <protein>corticosteroid receptors</protein> and that this reduction does increase plasma cortisol concentration , without affecting the glucocorticoid effector mechanism .

488

All-trans retinoic acid and 1 alpha , 25-dihydroxyvitamin D3 co-operate to promote differentiation of the human promyeloid leukemia cell line HL60 to monocytes .

All-trans retinoic acid and 1 alpha , 25-dihydroxyvitamin D3 co-operate to promote differentiation of the <cell_line>human promyeloid leukemia cell line</cell_line> <cell_line>HL60</cell_line> to <cell_type>monocytes</cell_type> .

489

A basis for differentiation therapy of leukemias is provided by knowledge of agents which induce specific lineage maturation .

490

All-trans retinoic acid ( RA ) induces differentiation of HL60 cells to neutrophils and is used to treat acute promyelocytic leukemia .

All-trans retinoic acid ( RA ) induces differentiation of <cell_line>HL60 cells</cell_line> to <cell_type>neutrophils</cell_type> and is used to treat acute promyelocytic leukemia .

491

We observed that RA did not induced neutrophil differentiation in serum-free grown HL60 cells whereas 50 nM 1 alpha , 25-dihydroxyvitamin D3 ( D3 ) induced maximal monocyte differentiation .

We observed that RA did not induced neutrophil differentiation in <cell_line>serum-free grown HL60 cells</cell_line> whereas 50 nM 1 alpha , 25-dihydroxyvitamin D3 ( D3 ) induced maximal monocyte differentiation .

492

Increasing RA concentrations reduced the D3 concentration required for monocyte differentiation .

493

Cells treated with 5 nM D3 showed little response , but differentiated maximally with 5 nM D3 and 10 nM RA .

494

The D3 analogs MC903 , EB1089 and KH1060 were more potent inducers of monocyte differentiation .

495

The extent to which analog activity was increased after cotreatment with RA was inversely related to potency .

496

Twenty-four hour treatment with 10 nM RA primed cells for response to 5 nM D3 ; the reverse sequence being ineffective .

Twenty-four hour treatment with 10 nM <cell_line>RA primed cells</cell_line> for response to 5 nM D3 ; the reverse sequence being ineffective .

497

Priming with 10 nM RA , or subsequent treatment with D3 ( 5 nM ) , did not alter expression of mRNAs encoding receptors for D3 ( VDR ) , RA ( RAR alpha ) or 9-CIS RA ( RXR alpha , beta , gamma ) .

Priming with 10 nM RA , or subsequent treatment with D3 ( 5 nM ) , did not alter expression of <rna>mRNAs</rna> encoding <protein>receptors</protein> for D3 ( <protein>VDR</protein> ) , RA ( <protein>RAR alpha</protein> ) or 9-CIS RA ( <protein>RXR alpha , beta , gamma</protein> ) .

498

That RA promotes both neutrophil and monocyte differentiation has implications for the use of RA and D3 in treatment of leukemias and provides insight into mechanisms whereby RAR , VDR and RXR facilitate monocyte differentiation .

That RA promotes both neutrophil and monocyte differentiation has implications for the use of RA and D3 in treatment of leukemias and provides insight into mechanisms whereby RAR , <protein>VDR</protein> and <protein>RXR</protein> facilitate monocyte differentiation .

499

[ An overexpression of retinoic acid receptor alpha blocks myeloid cell differentiation at the promyelocyte stage ]

[ An overexpression of <protein>retinoic acid receptor alpha</protein> blocks <cell_type>myeloid cell</cell_type> differentiation at the promyelocyte stage ]