{'fraction_non_alphanumeric': 0.02691065662002153, 'fraction_numerical': 0.014531754574811625, 'mean_word_length': 5.217391304347826, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 1, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Peptide:MHC Class II Presentation Infection Are Maintained by Low-Level T Cell Persistence and Function after + CD4

CD4 + memory–phenotype T cells decline over time when generated in response to acute infections cleared by other components of the immune system. Therefore, it was of interest to assess the stability of CD4 + T cells during a persistent Salmonella infection, which is typical of persistent phagocytic infections that are controlled by this lymphocyte subset. We found that CD4 + T cells speciﬁc for Salmonella peptide:MHC class II (MHCII) ligands were numerically stable for >1 y after initial oral infection. This stability was associated with peptide:MHCII-driven proliferation by a small number of T cells in the secondary lymphoid organs that harbored bacteria. The persistent population consisted of multifunctional Th1 cells that induced PD-1 and became exhausted when transferred to hosts expressing the speciﬁc peptide:MHCII ligand in all parts of the body. Thus, persistent infection of phagocytes produced a CD4 + T cell population that was stably maintained by low-level peptide:MHCII presentation. The Journal of Immunology , 2013, 190: 000–000. xpanded populations of Ag-speciﬁc T and B cells that persist long after pathogen clearance are responsible for immunological memory. These cells are useful to the host, providing protective immunity to subsequent challenge by the original microbe. The memory cell paradigm has been established most clearly for CD8 + T cells. CD8 + T cells expressing TCRs speciﬁc for microbe peptide:MHC class I (p:MHCI) ligands proliferate extensively, producing a peak number of effector cells about a week after acute infection. About 90% of these effector cells die by apoptosis, leaving a population of memory cells that is stably maintained by recurrent IL-15–driven homeostatic proliferation.