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The soluble cytoplasmic tail of CD45 regulates T-cell activation via TLR4 signaling. | LitMetric

AI Article Synopsis

  • * The study found that ct-CD45 activates TLR4 in Jurkat TLR4/CD14 reporter cells, leading to increased NFκB-eGFP expression, and this effect can be blocked by TLR4 inhibitors.
  • * Results suggest ct-CD45 uses a noncanonical pathway to modulate T cell receptor (TCR) signaling through TLR4, impacting T cell proliferation and function.

Article Abstract

The soluble cytoplasmic tail of CD45 (ct-CD45) is a cleavage fragment of CD45, that is generated during the activation of human phagocytes. Upon release to the extracellular space, ct-CD45 binds to human T cells and inhibits their activation in vitro. Here, we studied the potential role of TLR4 as a receptor for ct-CD45. Treatment of Jurkat TLR4/CD14 reporter cells with ct-CD45 induced the upregulation of the reporter gene NFκB-eGFP and could be blocked by inhibitors of TLR4 signaling. Conversely, ct-CD45 did not promote the NFκB-controlled eGFP induction in reporter cells expressing TLR1, TLR2, and TLR6 transgenes and did not lead to the activation of the transcription factors NFκB, AP-1, and NFAT in a Jurkat reporter cell line expressing endogenous TLR5. Moreover, ct-CD45 binds to recombinant TLR4 in an in vitro assay and this association was reduced in the presence of oxidized 1-palmitoyl-2-arachidonyl-sn-glycero-3-phosphorylcholine. Blockade of TLR4 with mAb HTA125 partially reversed the ct-CD45-mediated inhibition of T-cell proliferation. Interestingly, targeting of TLR4 with mAb W7C11 also suppressed T-cell proliferation. In summary, the results of this study demonstrate that ct-CD45 acts via a noncanonical TLR4 activation pathway on T cells, which modulates TCR signaling.

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Source
http://dx.doi.org/10.1002/eji.202149227DOI Listing

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