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Higher T cell activation in non‐obese diabetic/severe combined immunodeficient/interleukin‐2 (NOD/SCID/IL‐2) receptor ‐chainnull (NSG) mice transgenic for human stem cell factor (SCF) (NSG‐SGM3) mice humanized with human peripheral blood mononuclear cells (PBMC) (hu‐PBL‐NSG‐SGM3) HIV+ mice. (a) Expression of human leukocyte antigen D‐related (HLA‐DR) and CD38 and programmed cell death 1 (PD‐1) and inducible T cell co‐stimulator (ICOS) in CD8+ and CD4+ T cells from the seronegative and HIV‐infected donors. (b,c) Representative contour plots of the expression of HLA‐DR and CD38 and PD‐1 and ICOS in circulating CD8+ (b) and CD4+ T cells (c) from hu‐PBL‐NSG‐SGM3 HIV−, HIV+ untreated and HIV+ anti‐retroviral therapy (ART) mice at week 7 post‐engraftment. (d,e) Frequencies of HLA‐DR+CD38+, PD‐1+ and ICOS+CD8+ (d) and CD4+ T cells (e) from hu‐PBL‐NSG‐SGM3 HIV− (n = 10), HIV+ untreated (n = 3) and HIV+ ART (n = 9) mice throughout monitoring time. (c–e) *P ≤ 0·03 versus the other mouse groups, Kruskal–Wallis test. (d,e) The gray box indicates ART administration.

Journal: Clinical and Experimental Immunology

Article Title: High activation and skewed T cell differentiation are associated with low IL‐17A levels in a hu‐PBL‐NSG‐SGM3 mouse model of HIV infection

doi: 10.1111/cei.13416

Figure Lengend Snippet: Higher T cell activation in non‐obese diabetic/severe combined immunodeficient/interleukin‐2 (NOD/SCID/IL‐2) receptor ‐chainnull (NSG) mice transgenic for human stem cell factor (SCF) (NSG‐SGM3) mice humanized with human peripheral blood mononuclear cells (PBMC) (hu‐PBL‐NSG‐SGM3) HIV+ mice. (a) Expression of human leukocyte antigen D‐related (HLA‐DR) and CD38 and programmed cell death 1 (PD‐1) and inducible T cell co‐stimulator (ICOS) in CD8+ and CD4+ T cells from the seronegative and HIV‐infected donors. (b,c) Representative contour plots of the expression of HLA‐DR and CD38 and PD‐1 and ICOS in circulating CD8+ (b) and CD4+ T cells (c) from hu‐PBL‐NSG‐SGM3 HIV−, HIV+ untreated and HIV+ anti‐retroviral therapy (ART) mice at week 7 post‐engraftment. (d,e) Frequencies of HLA‐DR+CD38+, PD‐1+ and ICOS+CD8+ (d) and CD4+ T cells (e) from hu‐PBL‐NSG‐SGM3 HIV− (n = 10), HIV+ untreated (n = 3) and HIV+ ART (n = 9) mice throughout monitoring time. (c–e) *P ≤ 0·03 versus the other mouse groups, Kruskal–Wallis test. (d,e) The gray box indicates ART administration.

Article Snippet: For phenotypical analyses, whole blood samples were incubated for 30 min at room temperature with optimized doses of the following anti‐human antibodies: CD3‐fluorescein isothiocyanate (FITC) (clone HIT3a; BD Biosciences, San Jose, CA, USA), CD4‐BV421 (clone RPA‐T4; BD Biosciences), CD8‐Alexa Fluor (AF) 700 (clone OKT8; Thermo Fisher, Waltham, MA, USA), human leukocyte antigen D‐related (HLA‐DR)‐antigen‐presenting cells (APC)‐eFluor 780 (clone LN3; Thermo Fisher), CD38‐phycoerythrin (PE) eFluor 610 (clone HIT2; Thermo Fisher), programmed cell death 1 (PD‐1)‐BV510 (clone EH12.1; BD), inducible T cell co‐stimulator (ICOS) AF647 (clone DX29, BD), CCR7‐PE (clone 3D12; Thermo Fisher) and CD45RA‐PE cyanin 7 (Cy7) (clone HI100; Biolegend, San Diego, CA, USA).

Techniques: Activation Assay, Transgenic Assay, Expressing, Infection