- Email: [email protected]
Genomic organization of human 230-KD bullous pemphigoid antigen (BPAG1)
155 HINAJ
156 STIMULATORY
ACTTVlTY OF KRRATINOCYTE
GROWTH FACTOR ON MIGRATION
GROWTH
FACTORAND IIEI'ATOCYTE
AND CKLI. (;ROWTH LIF IlllMAN KEKATINOCYTE.
ACEW?JE SOLUBLE FRACTIONS K. SASAKI, M. UCXIYW?., ti.SUGIUR.??&DIl. UEHRPA, Department of Dematology, Shiga bniversity of Xedical Science, AND
Tsukinowa-cho,Seta, Otsu, Japan Fiwnandander often arovokesboth twze I and twe IV allergic responsesin-patientswith a‘topicdermatitis (AD). In this study, we examined relationshipbetween human dander antIyen fraction(s)For type I allergy and those for twx IV allersv in patientswith AD. Usmnq the water altile anj acetone sdiuble-fractions, scratch tests and patch tests w?re perfornlcd in 57 patientswith AD. The water soluble fractionoften provokedpxitlve scratch test reactions. However,the acetone soluble fractionconsx3xntly produceti negative scratch test responses.Roth fractionsoften producedposltlvepatch test reactions.Positivepatch test sites of the water soluble fractionhxstolcqxally shxed an eczematousreactionwith various munts of eosinopbils. But positivepatch test sites of the acetone soluble fraction reveal& Elieczematousresponstwith few eos~nop!nls.Thus, posltlvepatch test reactionsto acetone soluble fractionof numan dander hlstologlcallyres&led skin lesionsof AD.
157
K. SATO, H. TALUCHI
and K. YOSHIKAWA, Department of Dermatology, Osaka UrIiversity School of MrdicYne, l-1-50 Fukushima Fukushima-ku. Osaka. Japan we found that'riboflavinbecame cytotoxicafter Kecentlv, Pqrldouine, like ritu:lanear-u1;1-.iviolec iUVAi radiation. "in, has absorption in the range of UVA and is known to dechecked whether or "of Thus, compose after I_'\1 radiation. pyridoxinr became toxic to normal human, hydroa vacciniforme, and xeroderma pigmcntosum iibrotlasts in culture after UVA
we
radiation. CytOtuxiciCywas measuredby post-UVAcolony formation. The cells were killed by irradiation with EVA light Tclxicirv seemed to depend in the presence of pyridoxinr. mostly on the photoproduct af pvriduxine because the pyridovine solution chat had teen irradiated was toxic as much as The photo-induced roxicity of 6" min after UVA radiation. pyridoxine did not depend on excision repair since group A and C xeroderma pigmentosum fibroblasts were killed as the Sutrpidermal vesicular drrmarosis normal human fibroblssts. caused by pyridoxine described here.
+
could
be due
to the
toxicity
159 OF HUMAN 230-KD B"LL,o"S PEMPHIGOID ANTIGEN (BPAGl). D.SAWAMURA,~~-C.DO,K.TAMAI,K.I~I,J.UIT'IO,I.HASIIIMOTO. Dept.of Derm., Jefferson Medical Collage, USA, and Dept. of Derm. Hirosaki University, JAPAN.
GENOMIC
OHGANIZATION
exon-Intro" organization of the TO characterize entire BPAGI gene, a human genomic DNA library was Several clones spanning about screened with cDNA. 20 kb and corresponding to the entire coding Elucidation sequence of BPAGl were characterized.
of these clones indicated the 8kb coding region of BPAGl cDNA consisted of 22 separate exons, which varied from 78 to 2,730 bp in size. The 3'-end of the gene encoding the eight 3%residue repeat In contrast, region conslsted of one large exon. the sizes of multiple exons in the region coding for coiled-coil domain varied from 84 to 2,118 bp, while N-terminal globular domain was encoded by multiple relatively small axons. These results encoding functionally suggest the gene segments distinct domains in BPAGl have different structural organizations.
160 DISTRIBUTION OF COMPLEMENT REGULATORS (CD46, CD55 AND CD591 IN SKIN APPENDAGES AND SKIN NEOPLASMS S.SHIRAISHI AND Y.MIKI, Department of Ehime University School of Medicine, Shigenobucho, Onsengun, Ehime, Japan
K.SAYAMA,
Dermatology,
Immunohistochemical studies were performed to establish the distribution of membrane cofactor protein (MCP: CD46), decay-accelerating factor (D%.F: CD551 and homoloaous restriction factor IHRFZO: CD59) in normal Skin appendages, and in benign and malignant skin neoplasms. At least two of these regulators were detected on normal eccrine glands, apocrine glands and sebaceus glands. They were also found in cellular naevi, seborrheic keratoses, basal cell carcinoma, Bowen's disease, sequamous cell carcinoma and Paqet's disease. Although there were slight differences in their distribution, these regulators were found in all the cells examined, indicating that they are essential factors in human skin as well as other organs, and in neoplasms, in preventing autologous complement.
156 STIMULATORY
ACTTVlTY OF KRRATINOCYTE
GROWTH FACTOR ON MIGRATION
GROWTH
FACTORAND IIEI'ATOCYTE
AND CKLI. (;ROWTH LIF IlllMAN KEKATINOCYTE.
ACEW?JE SOLUBLE FRACTIONS K. SASAKI, M. UCXIYW?., ti.SUGIUR.??&DIl. UEHRPA, Department of Dematology, Shiga bniversity of Xedical Science, AND
Tsukinowa-cho,Seta, Otsu, Japan Fiwnandander often arovokesboth twze I and twe IV allergic responsesin-patientswith a‘topicdermatitis (AD). In this study, we examined relationshipbetween human dander antIyen fraction(s)For type I allergy and those for twx IV allersv in patientswith AD. Usmnq the water altile anj acetone sdiuble-fractions, scratch tests and patch tests w?re perfornlcd in 57 patientswith AD. The water soluble fractionoften provokedpxitlve scratch test reactions. However,the acetone soluble fractionconsx3xntly produceti negative scratch test responses.Roth fractionsoften producedposltlvepatch test reactions.Positivepatch test sites of the water soluble fractionhxstolcqxally shxed an eczematousreactionwith various munts of eosinopbils. But positivepatch test sites of the acetone soluble fraction reveal& Elieczematousresponstwith few eos~nop!nls.Thus, posltlvepatch test reactionsto acetone soluble fractionof numan dander hlstologlcallyres&led skin lesionsof AD.
157
K. SATO, H. TALUCHI
and K. YOSHIKAWA, Department of Dermatology, Osaka UrIiversity School of MrdicYne, l-1-50 Fukushima Fukushima-ku. Osaka. Japan we found that'riboflavinbecame cytotoxicafter Kecentlv, Pqrldouine, like ritu:lanear-u1;1-.iviolec iUVAi radiation. "in, has absorption in the range of UVA and is known to dechecked whether or "of Thus, compose after I_'\1 radiation. pyridoxinr became toxic to normal human, hydroa vacciniforme, and xeroderma pigmcntosum iibrotlasts in culture after UVA
we
radiation. CytOtuxiciCywas measuredby post-UVAcolony formation. The cells were killed by irradiation with EVA light Tclxicirv seemed to depend in the presence of pyridoxinr. mostly on the photoproduct af pvriduxine because the pyridovine solution chat had teen irradiated was toxic as much as The photo-induced roxicity of 6" min after UVA radiation. pyridoxine did not depend on excision repair since group A and C xeroderma pigmentosum fibroblasts were killed as the Sutrpidermal vesicular drrmarosis normal human fibroblssts. caused by pyridoxine described here.
+
could
be due
to the
toxicity
159 OF HUMAN 230-KD B"LL,o"S PEMPHIGOID ANTIGEN (BPAGl). D.SAWAMURA,~~-C.DO,K.TAMAI,K.I~I,J.UIT'IO,I.HASIIIMOTO. Dept.of Derm., Jefferson Medical Collage, USA, and Dept. of Derm. Hirosaki University, JAPAN.
GENOMIC
OHGANIZATION
exon-Intro" organization of the TO characterize entire BPAGI gene, a human genomic DNA library was Several clones spanning about screened with cDNA. 20 kb and corresponding to the entire coding Elucidation sequence of BPAGl were characterized.
of these clones indicated the 8kb coding region of BPAGl cDNA consisted of 22 separate exons, which varied from 78 to 2,730 bp in size. The 3'-end of the gene encoding the eight 3%residue repeat In contrast, region conslsted of one large exon. the sizes of multiple exons in the region coding for coiled-coil domain varied from 84 to 2,118 bp, while N-terminal globular domain was encoded by multiple relatively small axons. These results encoding functionally suggest the gene segments distinct domains in BPAGl have different structural organizations.
160 DISTRIBUTION OF COMPLEMENT REGULATORS (CD46, CD55 AND CD591 IN SKIN APPENDAGES AND SKIN NEOPLASMS S.SHIRAISHI AND Y.MIKI, Department of Ehime University School of Medicine, Shigenobucho, Onsengun, Ehime, Japan
K.SAYAMA,
Dermatology,
Immunohistochemical studies were performed to establish the distribution of membrane cofactor protein (MCP: CD46), decay-accelerating factor (D%.F: CD551 and homoloaous restriction factor IHRFZO: CD59) in normal Skin appendages, and in benign and malignant skin neoplasms. At least two of these regulators were detected on normal eccrine glands, apocrine glands and sebaceus glands. They were also found in cellular naevi, seborrheic keratoses, basal cell carcinoma, Bowen's disease, sequamous cell carcinoma and Paqet's disease. Although there were slight differences in their distribution, these regulators were found in all the cells examined, indicating that they are essential factors in human skin as well as other organs, and in neoplasms, in preventing autologous complement.