CD16 and CD57 Expressing Gamma Delta T Cells in Acute HIV-1 Infection are Associated with the Development of Neutralization Breadth
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PROVIDER: PRJNA1131432 | ENA |
REPOSITORIES: ENA
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Project description:New HIV vaccine approaches are focused on eliciting broadly neutralizing antibodies. We characterized early gamma-delta (γδ) T cell responses starting from pre-acquisition and during acute HIV infection (AHI) in participants previously characterized for neutralization breadth development. We found significant differences in γδ T cell surface marker expression in participants that developed neutralization breadth compared to those that did not. Activation of γδ T cells occurred within the first weeks of HIV acquisition and associated with viral load. Expression of CD16 on Vδ1 T cells and CD57 on Vδ2 T cells were found to be significantly higher in broad neutralizers during AHI, and associated with the development of neutralization breadth years later. In addition, the levels of CD16 on Vδ1 T cells was associated with early production of founder virus Env-specific IgM. Thus, γδ T cells may promote development of neutralization breadth, which has implications for HIV vaccine strategies.
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Project description:Gene-environment interactions are implicated in immunopathology, but few specific mechanisms have been identified. We defined two terminal-differentiation pathways for human CD4+ T cells each marked by CD57. Rare blood CD57+ CD4+ T cells marked by TCF1 downregulation (Thcyt) adopt a cytotoxic and terminal-effector transcriptome. By contrast, human CD57+ GC-Tfh cells exhibit a transcriptome of the precursor exhausted T cells marked by TCF7, TOX and ID3 and constitutive expression of CTLA4, which collectively confer resistance to becoming cytotoxic. By clarifying human CD4+ T cell terminal differentiation, we have revealed how CTLA4 mitigates the risk of maladaptive cytotoxicity during infection.
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Project description:Type 1 diabetes is an autoimmune disease in which insulin-secreting β cells of the pancreatic islets are selectively destroyed. CD8 T cells are regarded as critical players in mediating β cell destruction and as a result, considerable effort has been expended to define CD8 T cell behaviour in this disease. The overarching aim of the experiment is to characterize a recently identified autoreactive CD57-positive CD8 T cell subset which is associated with loss of function of islet beta cells in type 1 diabetes, to compare the phenotype of the CD57-positive effector memory CD8 T cells versus the CD57-negative compartment, and provide an insight into the function of these cells in the disease process. To that aim, HLA-A*24 positive patients with T1D -within 2 years of diagnosis- were asked to provide a blood, and following consent, and PBMC were isolated. CD57-positive and CD57-negative CD8 T cell populations were sorted by FACS, and finally, RNA was extracted. Amplified cDNA was obtained and used for the library preparation.
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Project description:Human peripheral blood monocytes (Mo) consist of subsets distinguished by expression of CD16 (FCGRIII) and chemokine receptors. Classical CD16- Mo express CCR2 and migrate in response to CCL2, while a minor CD16+ Mo subset expresses CX3CR1 and migrates into tissues expressing CX3CL1. CD16+ Mo produce pro-inflammatory cytokines and are expanded in certain inflammatory conditions including HIV infection. To gain insight into the developmental relationship and functions of CD16+ and CD16- Mo, we examined transcriptional profiles of these Mo subsets in peripheral blood from healthy individuals. Of 16,328 expressed genes, 2,759 genes were differentially expressed and 228 and 250 were >2-fold upregulated and downregulated, respectively, in CD16+ compared to CD16- Mo. CD16+ Mo were distinguished by upregulation of dendritic cell (DC) (SIGLEC10, CD43, RARA) and macrophage (MF) (CSF1R/CD115, MafB, CD97, C3aR) markers together with transcripts relevant for DC-T cell interaction (CXCL16, ICAM-2, LFA-1), cell activation (LTB, TNFRSF8, LST1, IFITM1-3, HMOX1, SOD-1, WARS, MGLL), and negative regulation of the cell cycle (CDKN1C, MTSS1), whereas CD16- Mo were distinguished by upregulation of myeloid (CD14, MNDA, TREM1, CD1d, C1qR/CD93) and granulocyte markers (FPR1, GCSFR/CD114, S100A8-9/12). Differential gene expression in CD16+ and CD16- Mo was confirmed by quantitative real time RT-PCR (i.e., CD16, C3AR1, C1QR1, ICAM-2, CSF1R, CSF3R, CDKN1C, TNFRSF1, and LTB) and flow cytometry (i.e., CSF1R, CSF3R, C1QR1, C3AR1, CD1d, CD43, CXCL16, and CX3CR1). Furthermore, increased expression of RARA and KLF2 transcripts in CD16+ Mo coincided with absence of cutaneous lymphocyte associated antigen (CLA) expression, indicating potential imprinting for non-skin homing. These results suggest that CD16+ and CD16- Mo originate from a common myeloid precursor, with CD16+ Mo having a more MF- and DC-like transcription program suggesting a more advanced stage of differentiation. Distinct transcriptional programs, together with their recruitment into tissues via different mechanisms, also suggest that CD16+ and CD16- Mo give rise to functionally distinct DC and MF in vivo.
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