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Blood, Vol. 95 No. 7 (April 1), 2000:
pp. 2386-2390
Variant genotypes of Fc RIIIA influence the
development of Kaposi's sarcoma in HIV-infected men
Thomas Lehr nbecher,
Charles B. Foster,
Shaoxian Zhu,
David Venzon,
Seth M. Steinberg,
Kathleen Wyvill,
Julia A. Metcalf,
Sandra S. Cohen,
Joseph Kovacs,
Robert Yarchoan,
Andrew Blauvelt, and
Stephen J. Chanock
From the Immunocompromised Host Section, Pediatric Oncology Branch;
Biostatistics and Data Management Section; HIV and AIDS Malignancy
Branch; and Dermatology Branch, National Cancer Institute; Laboratory
of Immunoregulation, National Institute of Allergy and Infectious
Diseases; and Critical Care Medicine Department, Clinical Center,
National Institutes of Health, Bethesda, MD.
Disturbances in inflammatory cytokine production and immune
regulation coupled with human herpesvirus-8 (HHV-8) infection underlie the current understanding of the pathogenesis of Kaposi's sarcoma (KS), the most common HIV-associated malignancy. The low affinity Fc gamma receptors (Fc R) for IgG link humoral and cellular immunity by mediating interaction between antibodies and effector cells, such as phagocytes and natural killer cells. We examined the
frequency of polymorphic forms of the low affinity
FcRs, FcRIIA,
FcRIIIA, and FcRIIIB in
2 cohorts of HIV-infected men with KS and found that the
FcRIIIA genotype exerts a significant influence
on susceptibility to or protection from KS. The FF genotype was
underrepresented in patients with KS, whereas the VF genotype was
associated with development of KS. A similar association was observed
between FcRIIIA genotypes and HHV-8
seropositivity. These observations suggest a possible role for
FcRIIIA in the development of KS during HIV infection.
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