By S. Holgate, et. al.
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Extra info for Allergy
Recent years have seen considerable progress in unravelling the contribution of specific genetic factors to an individual’s susceptibility, subsequent development, and severity of allergic disease. This has resulted in increasing insight into novel areas of allergic disease pathophysiology. Furthermore, studies of gene–environment interaction have lead to greater insight into the importance of environmental triggers for the initiation, exacerbation, and persistence of allergic diseases. Studies of the timing of action of genetic variants in determining disease susceptibility have highlighted the importance of in utero development and early life in determining susceptibility to allergic disease.
27 The structure of an integrin heterodimer with its α and β subunits. Examples of integrin heterodimers include: β1 integrins (α4β1 or VLA-4), β2 integrins (αLβ2 or LFA-1), and β7 integrins (α4β7). β2 integrins The β2 integrin subfamily is highly expressed on all circulating leukocytes and consists of a common β2 subunit (CD18) linked to one of four α subunits: CD11a, CD11b, CD11c, or CD11d. The leukocyte β2 integrins mediate firm adhesion of leukocytes to intercellular adhesion molecule-1 (ICAM-1) expressed by endothelial cells.
However, in a minority of subjects remodelling of tissues occur and this has been best studied in the lung in asthma. Apoptosis as a mechanism for resolution of inflammation Apoptosis and necrosis are two mechanisms by which cell death occurs. Apoptosis, or programmed cell death, is a mechanism for resolution of allergic or other forms of inflammation. Apoptotic cells are removed by neighboring phagocytic cells without loss of their potentially harmful cell contents. In contrast to apoptosis, necrosis is a pathological form of cell death resulting from acute cellular injury.