Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0220723 (
PCA
)
4,687
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The discovery of anaphylaxis by Portier and Richet that reinjection of a substance caused disease instead of immunity was sensational as it was against the prevailing DOGMA. Passive transmission of hypersensitivity with human antibody by Prausnitz (the P-K reaction, 1921) was an important step in the study of human hypersensitivity. Anaphylaxis was shown to be the consequence of liberation of vasoactive substances (histamine and SRS-A) from mast cells when the allergen crosslinks two IgE molecules fixed to mast cell Ig receptors (Ovary, 1961). The use of smooth muscle contraction (Dale, 1913) and vascular permeability increase (
PCA
, Ovary, 1948) became important for experimental studies. The clonal selection of antibody formation (Burnet, 1929) opened a new era in immunological concepts. The demonstration of the
Fc receptor
on mast cells (Ovary, 1961) called attention to the importance of cellular receptors. The carrier effect (Ovary & Benacerraf, 1963) was explained by recognition by T cell receptors of a processed carrier fragment complexed to Ia molecules (Unanue, Grey, 1981). Human IgE responsible for allergies was discovered in 1965 by K. & T. Ishizaka. Tonegawa in 1973 destroyed the "one gene-one protein" DOGMA, showing that the immunoglobulin, germline gene is discontinuous: i.e., composed of exons (which will form the Ig molecule) separated by introns. The CD4 cells were subdivided into Th1 and Th2 cells (Mosmann & Coffman, late 1980's). The Th2 secretes IL-4 necessary for IgE production (Paul, Vitetta, & others, early 1980's). B cells multiply before antibody production or become memory B cells, but what causes a B cell to become a memory cell is not known. The B cell does not change specificity but can switch the isotype using "switch recombinase" and the s segment of the Ig molecules (Honjo, early 1980's). IgE production was shown to be suppressed by lymphokines, such as IFN-gamma and IL-2. A great progress in understanding the mechanism of allergic reaction has been the result of intense investigations by many scientists. A more complete understanding, better prophylaxis and an improved treatment are the goals of the near future.
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PMID:Immediate hypersensitivity. A brief, personal history. 769 78