Atopic allergy: asthma and atopic dermatitis

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<ul><li><p>Of outstanding interest - in the opinion of immunologists. </p><p>Authors of reviews in the Current Opinion series of journals select from the previous years papers those they consider to be of outstanding interest. They justify each </p><p>selection in a short annotation. Some of the selected references from the December 1991 issue of Current Opinion in Immunology, which covers both Autoimmunity and </p><p>Atopic Allergy and Other Hypersensitivities, are listed below under the titles of the reviews. </p><p>A~~~~ Jkw: &amp;ma and atopic dermatitis by Thomas A.E. Platts-Mills </p><p>by A&amp; Y~JG S, VARNEY V, GAGA M, DURIN SR, MoQBEL %,w~w AJ, HAMID Q: Messenger RNA Expression of &amp; cytokine Gene Cluster, Interleukin-3 (IL-3), 1~14, d-5, and Granulocyte Macrophage Colony-stim- w ,Faaor, in Allergen-induced Late-phase Cuta- neous Reactions in Atopic Subjects. J Ex/, Med 1391, 173, 3:775-778. Biopsies of 24 h skin responses in atopic individuals dmtt-ate expression of cytokine genes of the K-3, IL- 4 and ~5 group. The results support the hypothesis that he T cells entering the skin in response to allergen ex- posure are compamble to the murine T helper type 2 subset-. </p><p>Cytokhe production by mast cells and bqsopbif?, by Stephen J. Galli, John R. Gordon and Barry K. Wershil </p><p>w&amp;@m BK, WANG Z, C~UXIN JR, GALI~ SJ: Recruit- ment * of Neutrophils During &amp;E-Dependent Cuta- neous Late pfiase Responses in the Mouse is Mast Cell Dependent: Partial Inhibition of the Reaction with A~~XYUI Against Tumor Necrosis Factor-Al- pha;&amp;lin invest 1991, 87446-453. First detionstration, using genetically mast-cell-deficient tie.,in..which the deliciency is overcome locally and ~electiveiy by adoptive transfer of in vitroderived mast @ls, that mast cells are essential for virtually all of the early and late phases of tissue swelling and leukocyte in f&amp;ration associated with IgEdependent reactions in the skin, and local administration of antibodies to TNF-~X can inhibit such mast-cell-dependent leukocyte infiltration by about 50%. This study presents the first direct evidence that a well characterized mast-cell-associated cytokine sig- wt&amp; influences the expression of an I@- and/or mast-cell-dependent biological response in viva. </p><p>W&amp;Q-I LJ, TRMMEIU G, WALDORF H&amp; WIUIAKEK D, MUW-IY GF: Human Dermal Mast Celis Contain and Release Tumor Necrosis Factor a which Induces En- dothew I-ahcyte Adhesion Molecule- 1. Proc Nat1 At.&amp; St2 lt.3 1991, 88:4220-4224. Demon.%f-ation using in situ hybridization that human deM mast ceUs represent the only ceU type in the normal dermis with detectable TNF-a immunoreactivity. </p><p>Volume 2 Number 2 1992 </p><p>Furthermore, some mast cells at sites of delayed hyper- sensitivity response express TNFa mRNA, and stimula- tion of put&amp;d dermal mast cells with morphine sul- fate results in loss of TNF-a immunoreactivity in the cells and the appearance of TNFa immunoreactivity in the cells supematant. Such mast-cell-derived TNF-a can in- duce ELM-1 expression by vascular endothelial cells. </p><p>IHJNG DYM, POBER JS, COTRAN RS: Expression of Endothelial-Leukocyte Adhesion Molecule-l in Elicited Late phase Allergic Reactions. J Cfin fnvtit 1991, 87:1805-1809. </p><p>Documents that injection of allergen into the skin of aller- gic subjects induces both EIAM-1 expression on vascular endothelial cells and leukocyte inliltration. Allergen also induces ELAM-1 expression on vascular endothelial cells in skin organ cultures in vitro, and this EIAh4-1 expres sion can be inhibited by combined treatment with anti- sera to TNF-a and IL-I, but not by antisera to either cy tokine alone. These findings support the conclusion that allergen-induced cytokine release by cells fixed in skin (probably mast cells), rather than by recruited cells, ac- counts for the augmented EIAM-1 expression observed during early phases of these responses. The relevant cy- tokines are likely to be TNFa and IL-l. </p><p>BOCHNEK BS, LUSCINSKA~ FW, GIMRRONE JA JR, N!SVMAN W, STERBINSKY SA, DERSE-ANTHONY CP, KUJM D, S~HLHMER RP: Adhesion of Human Basophils, Eosinophils, and Neutrophils to Interleukin I-Acti- vated Human Vascular Endothelial Cells: Contribu- tions of Endothelial Cell Adhesion Molecules. J E.@ Med 1991, 173:15531556. </p><p>In vitro assays of binding of human granulocytes to human umbilical vein endothelial cells, and flow cyto- metric detection of granulocyte counter-receptors for endothelial-ceU adhesion molecules, were used to sug- gest distinct roles for ICAMl, EM-1 and VCAh4-1 dur- ing granulocyte adhesion to vascular endothelium. Ba- sophils and eosinophils, unlike neutrophils, expressed very late antigen-4, the counter-receptor for VCAM-1, sug- gesting that preferential induction of VCAh4-1 on en- dothelial cells at sites of allergic responses might pro- mote the relatively selective recruitment of basophils and eosinophUs to these reactions. </p><p>73 </p></li></ul>