NKp30 and NKG2D contribute to natural killer recognition of HIV-infected cells.
| Title: | NKp30 and NKG2D contribute to natural killer recognition of HIV-infected cells. |
|---|---|
| Authors: | Zhao NQ; Pi R; Nguyen DN; Ranganath T; Seiler C; Holmes S; Marson A; Blish CA |
| Source: | BioRxiv : the preprint server for biology [bioRxiv] 2024 Jun 27. Date of Electronic Publication: 2024 Jun 27. |
| Publication Type: | Journal Article; Preprint |
| Language: | English |
| Journal Info: | Country of Publication: United States NLM ID: 101680187 Publication Model: Electronic Cited Medium: Internet ISSN: 2692-8205 (Electronic) Linking ISSN: 26928205 NLM ISO Abbreviation: bioRxiv Subsets: PubMed not MEDLINE |
| Abstract: | Natural killer (NK) cells respond rapidly in early HIV-1 infection. HIV-1 prevention and control strategies harnessing NK cells could be enabled by mechanistic understanding of how NK cells recognize HIV-infected T cells. Here, we profiled the phenotype of human primary NK cells responsive to autologous HIV-1-infected CD4 + T cells in vitro. We characterized the patterns of NK cell ligand expression on CD4 + T cells at baseline and after infection with a panel of transmitted/founder HIV-1 strains to identify key receptor-ligand pairings. CRISPR editing of CD4 + T cells to knockout the NKp30 ligand B7-H6, or the NKG2D ligands MICB or ULBP2 reduced NK cell responses to HIV-infected cells in some donors. In contrast, overexpression of NKp30 or NKG2D in NK cells enhanced their targeting of HIV-infected cells. Collectively, we identified receptor-ligand pairs including NKp30:B7-H6 and NKG2D:MICB/ULBP2 that contribute to NK cell recognition of HIV-infected cells. |
| Comments: | Update in: iScience. 2025 Sep 12;28(10):113548. doi: 10.1016/j.isci.2025.113548.. (PMID: 41079618) |
| Entry Date(s): | Date Created: 20240709 Date Completed: 20251021 Latest Revision: 20251021 |
| Update Code: | 20260130 |
| PubMed Central ID: | PMC11230221 |
| DOI: | 10.1101/2024.06.24.600449 |
| PMID: | 38979175 |
| Database: | MEDLINE |
Journal Article; Preprint