Disease relevance of Epa1

• High and low doses of haptens dictate whether dermal or epidermal antigen-presenting cells promote contact hypersensitivity [1].
• Ultraviolet radiation is known to induce a transient defect in epidermal antigen presentation which leads to the generation of antigen-specific suppression of the delayed-type hypersensitivity (DTH) response [2].
• The ability of epidermal antigen presenting cells (APC) to induce immune responses to herpes simplex virus (HSV) has been studied in mice of differing ages [3].

High impact information on Epa1

• IL-10 inhibits tumor antigen presentation by epidermal antigen-presenting cells [4].
• LCs are epidermal antigen-presenting dendritic cells that play important roles in skin immune responses [5].
• Four structurally related adhesins, Hwp1, Ala1p/Als5p, Als1p, from Candida albicans and Epa1p from Candida glabrata, are members of a class of proteins termed glycosylphosphatidylinositol-dependent cell wall proteins (GPI-CWP) [6].
• It also prevented the UV-induced suppression of epidermal antigen-presenting cell ability as measured by the mixed skin lymphocyte response [7].
• Co-incubation of epidermal cells in granulocyte-macrophage colony-stimulating factor and interleukin-1 alpha inhibited tumor-antigen presentation by epidermal antigen-presenting cells in this system and also inhibited alloantigen presentation in the primary mixed epidermal cell-lymphocyte reaction [8].

Chemical compound and disease context of Epa1

• Ultraviolet B (UVB) radiation is reported to induce a defect in epidermal antigen presentation which leads to specific suppression of the delayed-type hypersensitivity (DTH) response to trinitrochlorobenzene [9].
• Parallel recovery of epidermal antigen-presenting cell activity and contact hypersensitivity responses in mice exposed to ultraviolet irradiation: the role of a prostaglandin-dependent mechanism [10].

Biological context of Epa1

• Epa-1 is a tissue-restricted, non-major histocompatibility (MHC) antigen that may be responsible for the extreme sensitivity of skin to allograft rejection and graft-versus-host disease (GVHD), especially with MHC-compatible donors and recipients [11].
• High responses to Epa-1 were detected only in the H-2a and H-2k haplotypes; H-2b, H-2o1, H-2s, H-2t1, and H-2t2 haplotypes were nonresponders to Epa-1 [12].
• Epa-1 expression by PE M phi also could be induced in vivo by M phi-activating agents such as concanavalin A or Bacillus Calmette-Guérin (BCG), but not by the sterile inflammatory agents peptone broth or thioglycolate, suggesting a correlation between Epa-1 phenotype and M phi activation [13].

Anatomical context of Epa1

• Establishment of cytolytic T lymphocyte clones to epidermal alloantigen Epa-1 [14].
• I-A+ epidermal antigen-presenting cells (APCs, Langerhans cells) have been shown to present tumor-associated antigens (TAAs) and to induce tumor immunity in vivo [15].
• To confirm that Epa-1 serves as a target in allograft rejection and GVHD, we isolated Epa-1-specific cytotoxic T lymphocyte (CTL) clones completely in vivo from sponge-matrix allografts and from lymph nodes draining rejecting skin allografts [11].
• Cytotoxic T lymphocytes generated against epidermal alloantigen-1 (Epa-1), a tissue-restricted, non-H-2 alloantigen that is a target-cell determinant of both skin allograft rejection and cutaneous graft-versus-host reactions, directly produce full-thickness ulcerative skin lesions in Epa-1+ mice [16].
• Lysis of mouse macrophages, fibroblasts, and epidermal cells by epidermal alloantigen-specific cytotoxic T lymphocytes: effect of culture and inflammatory agents on Epa-1 expression [13].

Physical interactions of Epa1

• Cell-mediated cytotoxicity to nonmajor histocompatibility complex alloantigens on mouse epidermal cells. V. Contribution of bone marrow-derived cells to Epa-1 antigen expression [17].

Regulatory relationships of Epa1

• Interferon-gamma inhibits tumor antigen presentation by epidermal antigen-presenting cells [18].

Other interactions of Epa1

• However, the effects of interleukin-1 alpha and tumor necrosis factor-alpha differed with regard to presentation of tumor-associated antigens by epidermal antigen-presenting cells in a primed system [8].
• Compared to wild-type mice, a strongly enhanced expression level of interleukin-6 transcripts derived from epidermal antigen presenting cells were detected in the skin of IL-4 transgenic mice, whereas in the skin-draining lymph nodes of transgenic mice significantly lower levels were detected [19].
• The gene for a novel epidermal antigen maps near the neurofibromatosis 1 gene [20].
• From this and from parallel studies of spleen cell M phi it is concluded that Epa-1 may be a strain-specific marker for activated M phi in the mouse, as well as an inducible histocompatibility antigen in vivo [13].

References