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InVivoMab anti-mouse IFNAR-1 antibody

RRID:AB_2687723

Antibody ID

AB_2687723

Target Antigen

IFNAR-1 mouse

Proper Citation

(Bio X Cell Cat# BE0241, RRID:AB_2687723)

Clonality

monoclonal antibody

Comments

in vivo IFNAR-1 blockade, in vitro IFNAR-1 blockade

Clone ID

MAR1-5A3

Host Organism

mouse

Vendor

Bio X Cell Go To Vendor

Cat Num

BE0241 also BE0241-100MG, BE0241-1MG, BE0241-25MG, BE0241-50MG, BE0241-5MG, BP0241-100MG, BP0241-25MG, BP0241-50MG, BP0241-5MG

Publications that use this research resource

Self-Renewal and Toll-like Receptor Signaling Sustain Exhausted Plasmacytoid Dendritic Cells during Chronic Viral Infection.

  • Macal M
  • Immunity
  • 2018 Apr 17

Literature context:


Abstract:

Although characterization of T cell exhaustion has unlocked powerful immunotherapies, the mechanisms sustaining adaptations of short-lived innate cells to chronic inflammatory settings remain unknown. During murine chronic viral infection, we found that concerted events in bone marrow and spleen mediated by type I interferon (IFN-I) and Toll-like receptor 7 (TLR7) maintained a pool of functionally exhausted plasmacytoid dendritic cells (pDCs). In the bone marrow, IFN-I compromised the number and the developmental capacity of pDC progenitors, which generated dysfunctional pDCs. Concurrently, exhausted pDCs in the periphery were maintained by self-renewal via IFN-I- and TLR7-induced proliferation of CD4- subsets. On the other hand, pDC functional loss was mediated by TLR7, leading to compromised IFN-I production and resistance to secondary infection. These findings unveil the mechanisms sustaining a self-perpetuating pool of functionally exhausted pDCs and provide a framework for deciphering long-term exhaustion of other short-lived innate cells during chronic inflammation.

Funding information:
  • NEI NIH HHS - EY017478(United States)

TIM-3 Regulates CD103+ Dendritic Cell Function and Response to Chemotherapy in Breast Cancer.

  • de Mingo Pulido Á
  • Cancer Cell
  • 2018 Jan 8

Literature context:


Abstract:

Intratumoral CD103+ dendritic cells (DCs) are necessary for anti-tumor immunity. Here we evaluated the expression of immune regulators by CD103+ DCs in a murine model of breast cancer and identified expression of TIM-3 as a target for therapy. Anti-TIM-3 antibody improved response to paclitaxel chemotherapy in models of triple-negative and luminal B disease, with no evidence of toxicity. Combined efficacy was CD8+ T cell dependent and associated with increased granzyme B expression; however, TIM-3 expression was predominantly localized to myeloid cells in both human and murine tumors. Gene expression analysis identified upregulation of Cxcl9 within intratumoral DCs during combination therapy, and therapeutic efficacy was ablated by CXCR3 blockade, Batf3 deficiency, or Irf8 deficiency.

Funding information:
  • Intramural NIH HHS - DK015602-05(United States)
  • NCI NIH HHS - K99 CA185325()
  • NCI NIH HHS - P30 CA076292()
  • NCI NIH HHS - R00 CA185325()
  • NCI NIH HHS - R01 CA155331()
  • NCI NIH HHS - U54 CA163123()

Dichotomous Expression of TNF Superfamily Ligands on Antigen-Presenting Cells Controls Post-priming Anti-viral CD4+ T Cell Immunity.

  • Chang YH
  • Immunity
  • 2017 Nov 21

Literature context:


Abstract:

T cell antigen-presenting cell (APC) interactions early during chronic viral infection are crucial for determining viral set point and disease outcome, but how and when different APC subtypes contribute to these outcomes is unclear. The TNF receptor superfamily (TNFRSF) member GITR is important for CD4+ T cell accumulation and control of chronic lymphocytic choriomeningitis virus (LCMV). We found that type I interferon (IFN-I) induced TNFSF ligands GITRL, 4-1BBL, OX40L, and CD70 predominantly on monocyte-derived APCs and CD80 and CD86 predominantly on classical dendritic cells (cDCs). Mice with hypofunctional GITRL in Lyz2+ cells had decreased LCMV-specific CD4+ T cell accumulation and increased viral load. GITR signals in CD4+ T cells occurred after priming to upregulate OX40, CD25, and chemokine receptor CX3CR1. Thus IFN-I (signal 3) induced a post-priming checkpoint (signal 4) for CD4+ T cell accumulation, revealing a division of labor between cDCs and monocyte-derived APCs in regulating T cell expansion.

Funding information:
  • NIA NIH HHS - P01 AG017617(United States)