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APCS — CD4

Text-mined interactions from Literome

Hiltbold et al., J Immunol 2003 : Activation of CD4 ( + ) Th cells requires their cognate interaction with APCs bearing specific relevant MHC class II-peptide complexes
Burrows et al., Curr Drug Targets Inflamm Allergy 2005 (Autoimmune Diseases...) : Antigen presenting cells (APCs) initiate activation of CD4 ( + ) T cells in a multistep process that minimally involves co-ligation of the TCR and CD4 by the MHC class II/peptide complex and costimulation through additional T cell surface molecules such as CD28
Artis et al., J Immunol 2005 : In an in vivo adoptive transfer model in which NF-kappaB-sufficient OVA-specific DO11.10 TCR transgenic T cells were injected into OVA immunized WT or NF-kappaB1 ( -/- ) hosts, NF-kappaB1 ( -/- ) APCs efficiently promoted CD4 ( + ) T cell proliferation and IFN-gamma responses, but failed to promote Ag-specific IL-4 production
Alard et al., Diabetes 2006 (Diabetes Mellitus, Type 1...) : Surprisingly, stimulation of NOD CD4 ( + ) CD25 ( + ) cells with B6 APCs restored regulation, whereas with the reciprocal combination, NOD APCs failed to activate B6 CD4 ( + ) CD25 ( + ) cells properly
Guan et al., J Neuroimmunol 2007 (Disease Models, Animal...) : These APCs treated with M-CSF+autoantigen peptide significantly suppressed antigen-specific T cell proliferation, induced regulatory CD4 ( + ) and CD8 ( + ) T cells in vitro and in vivo, and significantly suppressed experimental autoimmune encephalomyelitis ( EAE )
Busch et al., J Immunol 2008 : Activation of CD4 ( + ) T cells by APCs occurs by multiple Ag recognition events including the exchange of costimulatory signals and cytokines
Lee et al., J Immunol 2009 : Furthermore, HBcAg-specific CD4 ( + ) and CD8 ( + ) T cell priming with DNA encoding HBcAg does not require B cell APCs
Brandler et al., J Virol 2010 : Antigen presenting cells (APCs) infected with MVA-HIV also activated HIV-specific CD4 ( + ) T cells
Wu et al., J Autoimmun 2011 (Encephalomyelitis, Autoimmune, Experimental) : These results indicate that DCs are capable of perpetuating CNS targeted autoimmunity when antigens are readily available, but other APCs are required to efficiently initiate pathogenic cognate CD4 T cell responses
Moses et al., J Exp Med 1990 : We found that ( a ) primary xenogeneic helper responses were absent, whereas primary allogeneic responses were brisk, ( b ) secondary xenogeneic helper responses were dependent on CD4+ T cells and responder antigen presenting cells (APCs), whereas allogeneic responses could be mediated by either CD4+ or CD8+ T cells independently and were primarily dependent on the presence of stimulator APCs , and ( c ) secondary xenogeneic helper responses were blocked by an antibody directed against responder class II MHC molecules
Feau et al., Nat Immunol 2011 (Listeriosis) : Our findings reconcile contradictory elements implicit in each model noted above by showing that CD4 ( + ) T cells activate APCs through a CD40L dependent mechanism to enable autocrine production of IL-2 in CD8 ( + ) memory T cells
Stanek et al., Mol Biotechnol 2012 : Complexes with biotinylated antibodies targeting cell surface receptors are formed and used to deliver the Ags of choice for processing and presentation by APCs and induction of Ag-specific CD4+ and CD8+ T-cell responses in vitro and in vivo
Ikejiri et al., Int Immunol 2012 : Naive CD4 ( + ) T cells are activated by antigen presenting cells (APCs) and differentiate into distinct types of helper T ( T ( h ) ) cells in the lymph node or spleen
Vlad et al., Exp Mol Pathol 2012 (Neoplasms) : Tolerogenic APCs induce CD4 ( + ) T helper anergy and elicit the differentiation of CD4 ( + ) and CD8 ( + ) T regulatory/suppressor cells