TY - CHAP
T1 - Antiphospholipid Antibodies and Their Relationship With Infections, Vaccines, and Drugs
AU - Ruiz, Jiram Torres
AU - Blank, Miri
AU - Zandman-Goddard, Gisele
AU - Sherer, Yaniv
AU - Shoenfeld, Yehuda
N1 - Publisher Copyright:
© 2016 Elsevier B.V.
PY - 2017
Y1 - 2017
N2 - Antiphospholipid antibodies (aPL) may accompany a response to many infectious agents. The emergence of aPL may be transient or associated with the clinical picture of antiphospholipid syndrome (APS) with thrombosis, recurrent foetal loss, central nervous system, and other organ involvement. The most studied pathogenic aPL antibodies are directed to the β2-glycoprotein-I (β2GPI) molecule. Studies on experimental APS models proved that molecular mimicry between β2GPI-related synthetic peptides and structures within bacteria, viruses, and tetanus toxoid can induce experimental APS. Any explanation of how microbial infections might trigger APS must take into account the observation that all individuals appear to harbour potentially autoreactive lymphocytes, as well as natural aPL, but they remain innocuous unless somehow activated by a second hit. In this chapter, we discuss the association of aPL with infections, vaccines, and drugs, with molecular mimicry as a proposed cause for the development of APS.
AB - Antiphospholipid antibodies (aPL) may accompany a response to many infectious agents. The emergence of aPL may be transient or associated with the clinical picture of antiphospholipid syndrome (APS) with thrombosis, recurrent foetal loss, central nervous system, and other organ involvement. The most studied pathogenic aPL antibodies are directed to the β2-glycoprotein-I (β2GPI) molecule. Studies on experimental APS models proved that molecular mimicry between β2GPI-related synthetic peptides and structures within bacteria, viruses, and tetanus toxoid can induce experimental APS. Any explanation of how microbial infections might trigger APS must take into account the observation that all individuals appear to harbour potentially autoreactive lymphocytes, as well as natural aPL, but they remain innocuous unless somehow activated by a second hit. In this chapter, we discuss the association of aPL with infections, vaccines, and drugs, with molecular mimicry as a proposed cause for the development of APS.
KW - Antiphospholipid antibody
KW - antiphospholipid syndrome
KW - drug
KW - infection
KW - vaccine
KW - β2 glycoprotein I
UR - http://www.scopus.com/inward/record.url?scp=85016710187&partnerID=8YFLogxK
U2 - 10.1016/B978-0-444-63655-3.00011-9
DO - 10.1016/B978-0-444-63655-3.00011-9
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AN - SCOPUS:85016710187
T3 - Handbook of Systemic Autoimmune Diseases
SP - 167
EP - 179
BT - Handbook of Systemic Autoimmune Diseases
PB - Elsevier Ltd.
ER -