Complement-Induced Granulocyte Aggregation: An Unsuspected Mechanism of Disease

Harry S Jacob, Mary Jean Moore, Dale E Hammerschmidt, Philip R. Craddock, Charles F. Moldow

Research output: Contribution to journalReview articlepeer-review

338 Scopus citations

Abstract

The capacity of blood cells to aggregate, best exemplified by the response of platelets to vascular injury, is generally thought to be beneficial. However, if aggregation occurs inappropriately—that is, in a manner irrelevant to hemostasis — ischemic syndromes may result. The myocardial ischemia of Prinzmetal's angina pectoris, for example, may reflect platelet aggregation in coronary arteries. This article presents evidence that granulocytes as well as platelets can aggregate intravascularly, and that the resultant and previously unsuspected phenomenon of leukoembolization may underlie tissue damage in such diverse clinical situations as pulmonary dysfunction in hemodialyzed patients, sudden blindness with retinal infarction after. . .

Original languageEnglish (US)
Pages (from-to)789-794
Number of pages6
JournalNew England Journal of Medicine
Volume302
Issue number14
DOIs
StatePublished - Apr 3 1980

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