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The second Aegean conference on 'Autoimmunity: Mechanisms and Novel Treatments' in September, 2005, discussed topics ranging from animal models of autoimmunity to lymphocyte interactions, as well as molecular influences of disease.
Precursors of specialized skin dendritic cells called Langerhans cells are derived from specific bone marrow–derived monocyte precursors that migrate to the skin and differentiate into these important immune surveillance cells.
Functional and phenotypic distinctions characterize B-1 cells versus B-2 cells. The identification of adult bone marrow cells that give rise exclusively to B-1 B cells support earlier ideas regarding the existence of dedicated B-1 progenitors.
It is unclear whether T cell exhaustion is reversible. A recent Nature paper shows that in vivo blockade of the inhibitory molecule PD-1 can restore the function of exhausted CD8+ T cells during chronic viral infection.
Lentiviral Nef protein has many functions in the evasion of host immune defenses. Another 'chink' in the host immune 'armor' has now been exposed by Nef's ability to inhibit immunoglobulin class switching.
The chemokine receptor CCR2 was believed to 'summon' infiltrating CCR2+ monocytes into the spleen. Instead, CCR2 seems to be important for 'release' of these cells from bone marrow niches.
Substitutions in CD8+ T cell epitopes in viral proteins can alter the complex interaction between viruses and host immunity. Reduced viral fitness and recognition of altered and subdominant epitopes are possible outcomes.
Suppressor of cytokine signaling 1 has been linked to the negative regulation of Toll-like receptor signaling. The mechanism for this seems to be suppressor of cytokine signaling 1–mediated degradation of the adaptor Mal, which is required for Toll-like receptor signaling.
Naive CD8+ T cells can be activated via dendritic cell 'cross-priming' of antigens obtained exogenously. Dendritic cells cannot cross-prime, however, after systemic activation in vivo, potentially contributing to immunosuppression associated with severe infections.
'Forward' genetic approaches for elucidating function can lead to unexpected findings. A single missense mutation is found to disrupt both antigen presentation and nucleic acid Toll-like receptor signaling, two processes involving endocytic pathways.
