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TGF-beta 1,-2,-3 MAb (Clone 1D11) antibody


Antibody ID


Target Antigen

TGF-beta 1-2-3 MAb (Clone 1D11) amoeba/protozoa, bovine, mollusc, hamster, sheep, chicken/bird, plant, porcine, c elegans/worm, drosophila/arthropod, other mammalian, xenopus/amphibian, donkey, goat, horse, mouse, rabbit, canine, feline, guinea pig, human, non-human primate, other invertebrate, reptile, bacteria/archaea, rat, multi-species

Proper Citation

(R and D Systems Cat# MAB1835, RRID:AB_357931)


monoclonal antibody


vendor recommendations: IgG1 Binding Inhibition, ELISA Capture (Matched Pair), Immunocytochemistry, Immunohistochemistry, Neutralization, Western Blot; Flow Cytometry; Block/Neutralize/Inhibit; ELISA; Immunohistochemistry; Western Blot; Immunocytochemistry

Host Organism



R and D Systems

Cat Num


Publications that use this research resource

RHOA G17V Induces T Follicular Helper Cell Specification and Promotes Lymphomagenesis.

  • Cortes JR
  • Cancer Cell
  • 2018 Feb 12

Literature context:


Angioimmunoblastic T cell lymphoma (AITL) is an aggressive tumor derived from malignant transformation of T follicular helper (Tfh) cells. AITL is characterized by loss-of-function mutations in Ten-Eleven Translocation 2 (TET2) epigenetic tumor suppressor and a highly recurrent mutation (p.Gly17Val) in the RHOA small GTPase. Yet, the specific role of RHOA G17V in AITL remains unknown. Expression of Rhoa G17V in CD4+ T cells induces Tfh cell specification; increased proliferation associated with inducible co-stimulator (ICOS) upregulation and increased phosphoinositide 3-kinase (PI3K) and mitogen-activated protein kinase signaling. Moreover, RHOA G17V expression together with Tet2 loss resulted in development of AITL in mice. Importantly, Tet2-/-RHOA G17V tumor proliferation in vivo can be inhibited by ICOS/PI3K-specific blockade, supporting a driving role for ICOS signaling in Tfh cell transformation.

Funding information:
  • NCI NIH HHS - R01 CA197945()
  • NIDDK NIH HHS - R37 DK44746(United States)

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:


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)

Diverse Requirements for Microglial Survival, Specification, and Function Revealed by Defined-Medium Cultures.

  • Bohlen CJ
  • Neuron
  • 2017 May 17

Literature context:


Microglia, the resident macrophages of the CNS, engage in various CNS-specific functions that are critical for development and health. To better study microglia and the properties that distinguish them from other tissue macrophage populations, we have optimized serum-free culture conditions to permit robust survival of highly ramified adult microglia under defined-medium conditions. We find that astrocyte-derived factors prevent microglial death ex vivo and that this activity results from three primary components, CSF-1/IL-34, TGF-β2, and cholesterol. Using microglial cultures that have never been exposed to serum, we demonstrate a dramatic and lasting change in phagocytic capacity after serum exposure. Finally, we find that mature microglia rapidly lose signature gene expression after isolation, and that this loss can be reversed by engrafting cells back into an intact CNS environment. These data indicate that the specialized gene expression profile of mature microglia requires continuous instructive signaling from the intact CNS.

Funding information:
  • NIDA NIH HHS - R01 DA015043()
  • NIMH NIH HHS - K08 MH112120()
  • NIMH NIH HHS - T32 MH019938()