Chapter 11 Antiphospholipid Antibodies, Infections, and Drugs

Miri Blank, Gisele Zandman Goddard, Yaniv Sherer, Yehuda Shoenfeld*

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review


Antiphospholipid antibodies (aPL) may accompany a response to many infectious agents. The emergence of aPL may be transient or may be associated with the clinical picture of the antiphospholipid syndrome (APS) with manifestations including thrombosis, recurrent fetal loss, central nervous system (CNS), and other organ involvement. The most studied pathogenic aPL are directed to the β2 glycoprotein I (β2GPI) molecule. Studies on experimental APS models have proved that molecular mimicry between β2GPI-related synthetic peptides and structures within bacteria, viruses, tetanus toxoid, and cytomegalovirus (CMV) can induce experimental APS. Any explanation of how microbial infections might set off APS must take into account the observation that all individuals appear to harbor potentially autoreactive lymphocytes, as well as natural aPL, but that these cells or antibodies remain innocuous unless somehow activated by a second hit. In this chapter we discuss the associations of aPL in infectious states, molecular mimicry as a proposed cause for the development of APS, aPL vaccination, and drug-induced aPL.

Original languageEnglish
Title of host publicationAntiphospholipid Syndrome in Systemic Autoimmune Diseases
EditorsRicard Cervera, Joan Carles Reverter, Munther Khamashta
Number of pages9
StatePublished - 2009
Externally publishedYes

Publication series

NameHandbook of Systemic Autoimmune Diseases
ISSN (Print)1571-5078


  • antiphospholipid antibodies
  • antiphospholipid syndrome
  • beta-2 glycoprotein I
  • drugs
  • infections


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