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The lack of visible pigment combines with defective cytotoxic T lymphocytes (CTLs) in a rare form of albinism called Hermansky-Pudlak Syndrome type 2. Griffiths and colleagues (p 1111; News and Views on p 1049) found a particular AP-3 mutant that both missorts tyrosinase in melanocytes and disables lytic granule transport to the immune synapse. Photomicrograph of CTL granules (green) and microtubules (red); clay sculpture by Lewis Long.
The immune system and the central nervous system operate in very different ways, but the dual use of the major histocompatibility complex for CD8+ T cell monitoring and pheromone presentation indicates some commonalities exist.
The importance of cross-priming in vivo is controversial because its relative contribution in the presence of conventional priming is unclear. However, data from the examination of a conserved tyrosine residue in the cytoplasmic tail of MHC class I favor the cross-priming hypothesis.
Patients with type 2 Hermansky-Pudlak syndrome are immunodeficient. Mutations in AP-3 that prevent movement of lytic granules along microtubules in CD8+ T cells help explain these patients' susceptibility to infection.
Tim-3, a member of the T cell immunoglobulin mucin family, is expressed by TH1 cells. Analysis of Tim-3–Tim3 ligand signaling now shows this pathway is intimately involved in the counter-regulation of T helper type 1 immune responses.
The LFA-1 integrin is known to mediate adhesion between T cells and antigen-presenting cells. New evidence, however, is provided for its role in transmitting signals that promote T cell activation and differentiation.