Journal
IMMUNOLOGY AND CELL BIOLOGY
Volume 94, Issue 8, Pages 729-740Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/icb.2016.42
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Funding
- National Health and Medical Research Council of Australia [5671222, APP1003131]
- NHMRC Project [1057707]
- NHMRC Principal Research Fellowship
- NHMRC Senior Principal Research Fellowship
- NHMRC Senior Research Fellowship
- National Health and Medical Research Council of Australia [1057707] Funding Source: NHMRC
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CD4 T follicular helper cells (TFH) are critical in the generation of potent and long-lived B-cell responses after viral infection. However, the factors that dictate the generation and maintenance of these cells are not fully understood. Here we use adoptive transfer of OTII T-cell receptor transgenic CD4 T cells, followed by infection with recombinant influenza A virus (IAV), as a means of identifying and tracking virus-specific CD4(+) T-cell responses. We show that T-cell competition within the virus-specific CD4 T-cell pool induced by IAV infection limits the proliferation and differentiation of IAV-specific CD4(+) TFH responses. In particular, increased T-cell competition for antigen results in a diminished IAV-specific TFH CD4 T-cell responses, particularly germinal center TFH responses. Strikingly, competition in the form of preexisting cellular immunity generated by heterosubtypic IAV immunization limits de novo CD4 T-cell responses in secondary lymphoid tissue. Taken together, these data show a profound linkage between antigen availability and promotion of TFH CD4(+) T-cell responses in response to infection. These data suggest that competition within the CD4 T-cell pool limits TFH responses and may be an important regulatory mechanism for controlling immunity.
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