TY - CHAP
T1 - Chapter 11 Antiphospholipid Antibodies, Infections, and Drugs
AU - Blank, Miri
AU - Zandman Goddard, Gisele
AU - Sherer, Yaniv
AU - Shoenfeld, Yehuda
PY - 2009/7/13
Y1 - 2009/7/13
N2 - 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.
AB - 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.
KW - antiphospholipid antibodies
KW - antiphospholipid syndrome
KW - beta-2 glycoprotein I
KW - drugs
KW - infections
UR - http://www.scopus.com/inward/record.url?scp=67649977557&partnerID=8YFLogxK
U2 - 10.1016/S1571-5078(08)00411-X
DO - 10.1016/S1571-5078(08)00411-X
M3 - Chapter
AN - SCOPUS:67649977557
SN - 9780444531698
T3 - Handbook of Systemic Autoimmune Diseases
SP - 139
EP - 147
BT - Antiphospholipid Syndrome in Systemic Autoimmune Diseases
A2 - Cervera, Ricard
A2 - Reverter, Joan Carles
A2 - Khamashta, Munther
ER -
