Ordered Just So: Lipid Rafts and Lymphocyte Function

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Science's STKE  05 Mar 2002:
Vol. 2002, Issue 122, pp. re2
DOI: 10.1126/stke.2002.122.re2


  • Fig. 1.

    Translocation of the BCR and TCR to lipid rafts may differ in how they are regulated. Lipid raft portions of the T cell or B cell plasma membrane are denoted in red; inactive Lck kinase is denoted by a boldface X. (A) For BCR engaging a high-affinity, high-valency antigen (Step 1), cross-linking of BCR by antigen may force a conformational change on oligomerized receptors (Step 2), which allows their translocation into lipid rafts, whereupon the Igα and Igβ signaling chains are phosphorylated by raft-localized Lyn and cross-linked to the actin cytoskeleton (Step 3). (B) For TCR engaging a lower affinity, low-valency antigen (Step 1), phosphorylation of the CD3 signaling chains is carried out by a pool of active Lck outside of lipid rafts, allowing fixation of the TCR to the actin cytoskeleton (Step 2), and subsequent translocation of fixed receptors into lipid rafts (Step 3).

  • Fig. 2.

    HIV subverts T cell lipid rafts at several stages of the viral life cycle. Lipid raft portions of the T cell membrane are indicated by red regions of the bilayer. HIV preferentially binds target cells at lipid rafts; viral replication is enhanced by T cell activation signal originating in lipid rafts; and viral budding takes place from within lipid rafts. Red arrows in the diagram indicate stages in the HIV life cycle where the raft-localized viral product Nef is thought to act to promote viral replication. (A) Nef is believed to enhance reverse transcription of viral RNA. (B) Lipid raft-localized Nef potentiates viral replication by (possibly) enhancing TCR signaling and by promoting IL-2 hyperresponsiveness. (C) Nef may promote viral assembly. Inset: Structural schematic of the mature HIV virus. CXCR, chemokine receptor. ssRNA, single stranded RNA.

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