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Stat5 (pY694) antibody

RRID:AB_10894188

Antibody ID

AB_10894188

Target Antigen

Stat5 (pY694) human

Proper Citation

(BD Biosciences Cat# 562077, RRID:AB_10894188)

Clonality

monoclonal antibody

Comments

Intracellular staining (flow Cytotoxicityometry)

Host Organism

mouse

Vendor

BD Biosciences Go To Vendor

Cat Num

562077

Publications that use this research resource

CRIg, a tissue-resident macrophage specific immune checkpoint molecule, promotes immunological tolerance in NOD mice, via a dual role in effector and regulatory T cells.

  • Yuan X
  • Elife
  • 2017 Nov 24

Literature context:


Abstract:

How tissue-resident macrophages (TRM) impact adaptive immune responses remains poorly understood. We report novel mechanisms by which TRMs regulate T cell activities at tissue sites. These mechanisms are mediated by the complement receptor of immunoglobulin family (CRIg). Using animal models for autoimmune type 1 diabetes (T1D), we found that CRIg+ TRMs formed a protective barrier surrounding pancreatic islets. Genetic ablation of CRIg exacerbated islet inflammation and local T cell activation. CRIg exhibited a dual function of attenuating early T cell activation and promoting the differentiation of Foxp3+ regulatory (Treg) cells. More importantly, CRIg stabilized the expression of Foxp3 in Treg cells, by enhancing their responsiveness to interleukin-2. The expression of CRIg in TRMs was postnatally regulated by gut microbial signals and metabolites. Thus, environmental cues instruct TRMs to express CRIg, which functions as an immune checkpoint molecule to regulate adaptive immunity and promote immune tolerance.

Funding information:
  • NIGMS NIH HHS - T32 GM07270(United States)

CTLA-4+PD-1- Memory CD4+ T Cells Critically Contribute to Viral Persistence in Antiretroviral Therapy-Suppressed, SIV-Infected Rhesus Macaques.

  • McGary CS
  • Immunity
  • 2017 Oct 17

Literature context:


Abstract:

Antiretroviral therapy (ART) suppresses viral replication in HIV-infected individuals but does not eliminate the reservoir of latently infected cells. Recent work identified PD-1+ follicular helper T (Tfh) cells as an important cellular compartment for viral persistence. Here, using ART-treated, SIV-infected rhesus macaques, we show that CTLA-4+PD-1- memory CD4+ T cells, which share phenotypic markers with regulatory T cells, were enriched in SIV DNA in blood, lymph nodes (LN), spleen, and gut, and contained replication-competent and infectious virus. In contrast to PD-1+ Tfh cells, SIV-enriched CTLA-4+PD-1- CD4+ T cells were found outside the B cell follicle of the LN, predicted the size of the persistent viral reservoir during ART, and significantly increased their contribution to the SIV reservoir with prolonged ART-mediated viral suppression. We have shown that CTLA-4+PD-1- memory CD4+ T cells are a previously unrecognized component of the SIV and HIV reservoir that should be therapeutically targeted for a functional HIV-1 cure.

Funding information:
  • CCR NIH HHS - HHSN261200800001C()
  • NCI NIH HHS - HHSN261200800001E()
  • NHGRI NIH HHS - P01 HG004120(United States)
  • NIAID NIH HHS - P30 AI050409()
  • NIAID NIH HHS - R01 AI110334()
  • NIAID NIH HHS - R01 AI116379()
  • NIAID NIH HHS - R33 AI104278()
  • NIAID NIH HHS - R33 AI116171()
  • NIH HHS - P51 OD011132()