X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Phospho-NFkB p65 (Ser529) Monoclonal Antibody (B33B4WP), eFluor 660, eBioscience(TM)

RRID:AB_2574397

Antibody ID

AB_2574397

Target Antigen

Phospho-NFkB p65 (Ser529) See NCBI gene human

Proper Citation

(Thermo Fisher Scientific Cat# 50-9863-42, RRID:AB_2574397)

Clonality

monoclonal antibody

Comments

Applications: Flow (5 µL (0.06 µg)/test)

Clone ID

Clone B33B4WP

Host Organism

mouse

Vendor

Thermo Fisher Scientific Go To Vendor

Cat Num

50-9863-42 also 50-9863

Publications that use this research resource

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)