Advances in basic and clinical immunology in 2007

In 2007, there was significant progress in the area of basic immunology, including investigations that led to a better understanding of the function of antigen-presenting cells, such as the secretion of cytokines that inhibit or induce allergic inflammation on antigen stimulation. Mechanisms of IgE function were better characterized, and the clonality of IgE-producing B cells in allergic responses of monosensitized patients was demonstrated. The hygiene hypothesis was re-examined, with most of the evidence suggesting that the increase of atopy prevalence is best explained by the absence of TH1 responses rather than the absence of regulatory T cells. The effects of the environment in the allergic inflammation of the lung received new emphasis. Similar progress took place in the area of clinical immunology. Immune adverse reactions to drugs, such as the toxicity of carbamazepine-specific T cells and the safety and efficacy of drugs for the treatment of hereditary angioedema, were better characterized. There were advances in the molecular characterization of primary immunodeficiencies and their management, remarkably the discovery of signal transducer and activator of transcription 3 gene mutations as the cause of hyper-IgE syndrome. Long-term outcomes of bone marrow transplantation for severe combined immunodeficiencies confirmed the efficacy of this therapy.

Key words: Basic immunology, antigen presentation, IgE, regulatory T cells, lung immunology, clinical immunology, immunodeficiency, hereditary angioedema, mastocytosis, common variable immunodeficiency, HIV infection

Abbreviations used: BMT, Bone marrow transplantation, CVID, Common variable immunodeficiency, DC, Dendritic cell, HAE, Hereditary angioedema, HIES, Hyper-IgE syndrome, NK, Natural killer, SOCS, Suppressor of cytokine signaling, STAT, Signal transducer and activator of transcription, TACI, Transmembrane activation and calcium modulation cyclophilin interactor, TLR, Toll-like receptor