OX40 controls effector CD4+ T-cell expansion, not follicular T helper cell generation in acute Listeria infection.
Bottom Line: Mice deficient in OX40 and CD30 showed normal generation of TFH cells but impaired numbers of 2W1S-specific effector cells.OX40 was not expressed by 2W1S-specific memory cells, although it was rapidly up-regulated upon challenge whereupon Ab-ligation of OX40 specifically affected the effector subset.In summary, these data indicate that for CD4(+) T cells, OX40 signals are important for generation of effector T cells rather than TFH cells in this response to acute bacterial infection.
Affiliation: MRC Centre for Immune Regulation, Institute for Biomedical Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.Show MeSH
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Mentions: To further investigate whether OX40 signals were required for the formation of TFH cells in the response to Lm-2W, mice deficient in both OX40 and CD30 were used, since there may be redundancy in these signalling pathways 8. WT and CD30−/−OX40−/− mice were immunised with Lm-2W and then analysed at 7 dpi. An overall decrease in the number of CD44hi2W1S:I-Ab+CD4+ T cells (Supporting Information Fig. 2; p = 0.0317; median for WT: 52 331, CD30−/−OX40−/−: 21 975) resulted from less CXCR5− effector cells (p = 0.0159; median for WT: 27 164, CD30−/−OX40−/−: 8103) consistent with decreased survival, however generation of TFH was not impaired (p = 0.5556; median for WT: 2850, CD30−/−OX40−/−: 3430), indicating that the generation of these cells did not require OX40 signals.
Affiliation: MRC Centre for Immune Regulation, Institute for Biomedical Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.