| First Author | Wikenheiser DJ | Year | 2018 |
| Journal | Front Immunol | Volume | 9 |
| Pages | 2277 | PubMed ID | 30374346 |
| Mgi Jnum | J:313189 | Mgi Id | MGI:6791560 |
| Doi | 10.3389/fimmu.2018.02277 | Citation | Wikenheiser DJ, et al. (2018) NK1.1 Expression Defines a Population of CD4(+) Effector T Cells Displaying Th1 and Tfh Cell Properties That Support Early Antibody Production During Plasmodium yoelii Infection. Front Immunol 9:2277 |
| abstractText | Early plasmablast induction is a hallmark of Plasmodium infection and is thought to contribute to the control of acute parasite burden. Although long understood to be a T-cell dependent phenomenon, regulation of early plasmablast differentiation, however, is poorly understood. Here, we identify a population of CD4(+) T cells that express the innate NK cell marker NK1.1 as an important source of T cell help for early plasmablast and parasite-specific Ab production. Interestingly, NK1.1(+) CD4(+) T cells arise from conventional, naive NK1.1(-) CD4(+) T cells, and their generation is independent of CD1d but critically reliant on MHC-II. CD4(+) T cells that express NK1.1 early after activation produce IFN-gamma and IL-21, and express the follicular helper T (Tfh) cell markers ICOS, PD-1 and CXCR5 more frequently than NK1.1(-) CD4(+) T cells. Further analysis of this population revealed that NK1.1(+) Tfh-like cells were more regularly complexed with plasmablasts than NK1.1(-) Tfh-like cells. Ultimately, depletion of NK1.1(+) cells impaired class-switched parasite-specific antibody production during early Plasmodium yoelii infection. Together, these data suggest that expression of NK1.1 defines a population of rapidly expanding effector CD4(+) T cells that specifically promote plasmablast induction during Plasmodium infection and represent a subset of T cells whose modulation could promote effective vaccine design. |
