Titlebook: Immunodermatology; Bijan Safai,Robert A. Good Book 1981 Springer Science+Business Media New York 1981 antibody.asthma.dermatology.diseases

灾难

Natural Control over Immune Responses,cell-mediated and humoral activities, involves a complex web of cellular interactions recently described by Jerne (1974) as a “network.” These interactions include a number of stop-and-go signals mediated by various leukocytes and their circulating soluble products. Specificity of these regulatory a

尖

MAOIS

土产

Role of Proteinases in Cutaneous Inflammation,al cells are phagocytic, and proteinases are necessary for digestion of endocytosed exogenous proteins (Nordquist .., 1966; Wolff and Schreiner, 1969; Wolff and Honigsmann, 1968, Wolff and Konrad, 1972). Proteinases also play a role in the programmed catabolism associated with keratinization (Lazaru

Afflict

抗生素

朝圣者

Adverse Drug Reactions,llowing penicillin administration is the best example of such a reaction. An adverse reaction may also result when a drug is used as a preservative, as a filler, or as a dye or stabilizer in preparing another drug, food, or cosmetic. These reactions are usually classified as allergic or nonallergic.

带伤害

The Graft-vs.-Host Reaction in Man,immunologically unable to react against foreign cells. Under experimental conditions, GVHR can be induced when immunologically competent cells are transferred to a recipient unresponsive because of immunological immaturity (e.g., newborn mice) or immunosuppressive therapy (e.g., following total-body

显微镜

Allergic Contact Dermatitis, Photoallergic Contact Dermatitis, and Phototoxic Dermatitis,acteristic changes in the epidermis and dermis evoked by this perhaps most uniquely “cutaneous” immunological response. Its historical interest derives from the fact that some of the first recognized cardinal clinical features of immune responses in man can be traced to ACD. These include the clear-

Sigmoidoscopy

Urticaria/Angioedema,m the antigen-induced release of biologically active materials from mast cells sensitized with specific IgE antibody. In humans, the clinical symptom complex occurs rapidly after the exposure of a sensitive individual to the appropriate antigen. The sites of clinical expressions include the skin (ur