Abstract

Epidermal Langerhans cells resemble macrophages/monocytes in several remarkable ways: both bear surface receptors for the Fc portion of immunoglobulin molecules and for the C3b complement component. They take up, process and present antigen to reactive lymphocytes in an extremely effective fashion. They display on their cell surfaces the alloantigenic determinants encoded by genes of the I region of the major histocompatibility complex. Using ATPase activity, Langerhans cell surface densities are abnormal in 3 cutaneous sites which exhibit unique immunologic properties: markedly reduced numbers in hamster cheek pouch; reduced numbers and uneven distributions in murine tail skin; no Langerhans cells occur within corneal epithelium. As a functional expression of the absence of Langerhans cells from murine corneas, allografts prepared from corneal epithelium fail to sensitize recipients to Ia antigens encoded by I region genes of the donor. Corneal grafts disparate from their hosts at only I region loci are accepted for at least 45 days. The absence of Langerhans cells from cornea may account in part for its property as an immunologically privileged tissue. Subthreshold numbers of Langerhans cells in cheek pouch epithelium may contribute significantly to the observations that the hamster cheek pouch is an immunologically privileged site. We infer that skin deficient in Langerhans cells may be consequently deficient in alloantigenicity. Equally important, Langerhans cell-poor skin may be lacking in certain essential functions relating to the induction and expression of immune reactivity.

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