MOUSE ANTI RAT CD4 (DOMAIN 2) Azide Free

Price:
889 EUR
1066 USD
737 GBP
known as: MOUSE ANTI RAT CD4 (DOMAIN 2) Azide Free
Catalog number: genta-ABS0370
Product Quantity: 1 mg
Category:
Supplier: AbD

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Gene target: cd4 domain 2

Related genes to: MOUSE ANTI RAT CD4 (DOMAIN 2) Azide Free

Symbol : cd4 NIH gene
description : T-cell surface glycoprotein CD4
type of gene : protein-coding
Modification date : 2015-09-26

Related Pathways to: MOUSE ANTI RAT CD4 (DOMAIN 2) Azide Free

Gene about :domain
Pathway :Dm Notch Signaling Pathway
domain
Gene about :Cd4
Pathway :Rn Cytokines and Inflammatory Response (BioCarta)
Cd4

Related product to: MOUSE ANTI RAT CD4 (DOMAIN 2) Azide Free

Related Articles about: MOUSE ANTI RAT CD4 (DOMAIN 2) Azide Free

IFNγ-producing CD4(+) T lymphocytes: the double-edged swords in tuberculosis.

IFNγ-producing CD4(+) T cells (IFNγ(+)CD4(+) T cells) are the key orchestrators of protective immunity against Mycobacterium tuberculosis (Mtb). Primarily, these cells act by enabling Mtb-infected macrophages to enforce phagosome-lysosome fusion, produce reactive nitrogen intermediates (RNIs), and activate autophagy pathways. However, TB is a heterogeneous disease and a host of clinical and experimental findings has also implicated IFNγ(+)CD4(+) T cells in TB pathogenesis. High frequency of IFNγ(+)CD4(+) T cells is the most invariable feature of the active disease. Active TB patients mount a heightened IFNγ(+)CD4(+) T cell response to mycobacterial antigens and demonstrate an IFNγ-inducible transcriptomic signature. IFNγ(+)CD4(+) T cells have also been shown to mediate TB-associated immune reconstitution inflammatory syndrome (TB-IRIS) observed in a subset of antiretroviral therapy (ART)-treated HIV- and Mtb-coinfected people. The pathological face of IFNγ(+)CD4(+) T cells during mycobacterial infection is further uncovered by studies in the animal model of TB-IRIS and in Mtb-infected PD-1(-/-) mice. This manuscript encompasses the evidence supporting the dual role of IFNγ(+)CD4(+) T cells during Mtb infection and sheds light on immune mechanisms involved in protection versus pathogenesis. - Source :PubMed

CD4 T Cells in IBD: Crossing the Line?

- Source :PubMed

Loss of Gαi proteins impairs thymocyte development, disrupts T-cell trafficking, and leads to an expanded population of splenic CD4(+)PD-1(+)CXCR5(+/-) T-cells.

Thymocyte and T cell trafficking relies on signals initiated by G-protein coupled receptors. To address the importance of the G-proteins Gαi2 and Gαi3 in thymocyte and T cell function, we developed several mouse models. Gαi2 deficiency in hematopoietic progenitors led to a small thymus, a double negative (DN)1/DN2 thymocyte transition block, and an accumulation of mature single positive (SP) thymocytes. Loss at the double positive (DP) stage of thymocyte development caused an increase in mature cells within the thymus. In both models an abnormal distribution of memory and naïve CD4 T cells occurred, and peripheral CD4 and CD8 T cells had reduced chemoattractant responses. The loss of Gαi3 had no discernable impact, however the lack of both G-proteins commencing at the DP stage caused a severe T cell phenotype. These mice lacked a thymic medullary region, exhibited thymocyte retention, had a peripheral T cell deficiency, and lacked T cell chemoattractant responses. Yet a noteworthy population of CD4(+)PD-1(+)CXCR5(+/-) cells resided in the spleen of these mice likely due to a loss of regulatory T cell function. Our results delineate a role for Gαi2 in early thymocyte development and for Gαi2/3 in multiple aspects of T cell biology. - Source :PubMed

Concurrent OX40 and CD30 Ligand Blockade Abrogates the CD4-Driven Autoimmunity Associated with CTLA4 and PD1 Blockade while Preserving Excellent Anti-CD8 Tumor Immunity.

Although strategies that block FOXP3-dependent regulatory T cell function (CTLA4 blockade) and the inhibitory receptor PD1 have shown great promise in promoting antitumor immune responses in humans, their widespread implementation for cancer immunotherapy has been hampered by significant off-target autoimmune side effects that can be lethal. Our work has shown that absence of OX40 and CD30 costimulatory signals prevents CD4 T cell-driven autoimmunity in Foxp3-deficient mice, suggesting a novel way to block these side effects. In this study, we show that excellent antitumor CD8 T cell responses can be achieved in Foxp3(KO) mice deficient in OX40 and CD30 signals, particularly in the presence of concurrent PD1 blockade. Furthermore, excellent antitumor immune responses can also be achieved using combinations of Abs that block CTLA4, PD1, OX40, and CD30 ligands, without CD4 T cell-driven autoimmunity. By dissociating autoimmune side effects from anticancer immune responses, this potentially shifts this antitumor approach to patients with far less advanced disease. - Source :PubMed

Attenuated IL-2R signaling in CD4 memory T cells of T1D subjects is intrinsic and dependent on activation state.

The IL-2/IL-2R pathway is implicated in type 1 diabetes (T1D). While its role in regulatory T cell (Treg) biology is well characterized, mechanisms that influence IL-2 responses in effector T cells (Teff) are less well understood. We compared IL-2 responses in 95 healthy control and 98 T1D subjects. In T1D, low IL-2 responsiveness was most pronounced in memory Teff. Unlike Treg, CD25 expression did not influence the Teff responses. Reduced IL-2 responses in memory Teff were not rescued by resting, remained lower after activation and proliferation, and were absent in type 2 diabetes. Comparing basal IL-2 responses in resting versus activated cells, memory Teff displayed lower, but more sustained, responses to IL-2 overtime. These results suggest that T1D-associated defects in the Teff compartment are due to intrinsic factors related to activation. Evaluation of both Teff and Treg IL-2R signaling defects in T1D subjects may inform selection of therapies. - Source :PubMed

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