Membrane domains and the immunological synapse: keeping T cells resting and ready - PubMed (original) (raw)

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Membrane domains and the immunological synapse: keeping T cells resting and ready

Michael L Dustin. J Clin Invest. 2002 Jan.

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Figure 1

Figure 1

Regulation of Lck by rafts and Cbp. Cbp is localized to rafts in resting cells, where it is phosphorylated by active Lck*, an Src family PTK. This modification recruits Csk, which inactivates Lck† by phosphorylating its C-terminal regulatory site, and PEP, which dephosphorylates the Lck activation loop. Another phosphatase, CD45, is localized outside the rafts but may have access to Lck at the lateral boundary or during rare meetings due to partitioning into the same membrane domain. Activation of the TCR results in dephosphorylation of Cbp through the action of an unidentified phosphatase, thus removing the inhibitory complex containing Csk and PEP.

Figure 2

Figure 2

Hypothesis for agrin regulation of immunological synapse formation. (a) Raft-aggregating activity of agrin proteoglycan is regulated by intramolecular interaction with heparan sulfate chains. (b) When these chains are degraded by the lymphocyte heparanase, the raft-aggregating activity is expressed. (c) Recent evidence indicates that T cell agrin glycoprotein (agrinact) enhances synapse formation and T cell activation. Conversely, if agrin glycoprotein is prevented from entering the synapse, perhaps through an interaction with laminin or other ECM components, the formation of the synapse may be destabilized by ectopic raft aggregates, thus preventing T cell activation. Thus, in the presence of specific ECM components, the effect of actin conversion from proteoglycan to glycoprotein may be inhibitory, whereas in an ECM-depleted site like a lymph node it may enhance responses.

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References

    1. Katz JD, Wang B, Haskins K, Benoist C, Mathis D. Following a diabetagenic T cell from genesis through pathogenesis. Cell. 1993;74:1089–1100. - PubMed
    1. Lafaille JJ, Nagashima K, Katsuki M, Tonegawa S. High incidence of spontaneous autoimmune encephalomyelitis in immunodeficient anti-myelin basic protein T cell receptor transgenic mice. Cell. 1994;78:399–408. - PubMed
    1. Peterson DA, DiPaolo RJ, Kanagawa O, Unanue ER. Negative selection of immature thymocytes by a few peptide-MHC complexes: differential sensitivity of immature and mature T cells. J Immunol. 1999;162:3117–3120. - PubMed
    1. Alam SM, et al. T-cell-receptor affinity and thymocyte positive selection. Nature. 1996;381:616–620. - PubMed
    1. Williams CB, Engle DL, Kersh GJ, Michael White J, Allen PM. A kinetic threshold between negative and positive selection based on the longevity of the T cell receptor-ligand complex. J Exp Med. 1999;189:1531–1544. - PMC - PubMed

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