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196 Liver-derived T cell clones in autoimmune chronic active hepatitis
1%
196
WITHDRAWN
LIVER-DERIVED T CELL CLONES IN AUTOIMMUNE CHRONIC ACTIVE HEPATITIS V. Barnaba, A. France, G. Ruberti, R. Benvenuto, C. Balsano, F. Balsano. Istituto I Clinica Medica, Universita "La Sapienza", Rome, Italy. 22 T cell clones expanded with PHA, rIL2 and irra diated autologous PBMC were generated by a liver derived T cell line recognizing autologous hepatE cytes expressing class II MHC antigens. 12 clones were CD3/CD8+ and 10 clones were CD3/CD4+. All clones resulted DR+ and TAC+ but none expressed CD16 or ~~11 molecules. 4 out of the CD8+ and 3 out of CD4+ T cell clones proliferated to autologous hepatocytes but not to irradiated autologous PBMC or HLA-DR+ allogeneic hepatocytes: anti-class II MoAb blocked the CD4+ clones proliferation against autologous hepatocytes as well as anti-class I MoAb blocked the CD8+ proliferation against autologous hepatocytes. All the CD8+ clones and 5 out of 10 CD4+ clones expressed CTL activity evaluated by lectin-Dependent-Cytotoxicity (LDCC). 10 out of 12 CD8+ clones and 3 out of 10 CD4+ clones showed NK activity against K562 cell line. 3 out of these10 CD8+ clones had cytotoxic activity against an human hepatocarcinoma cell line (PLC/PRF/5), producing HBsAg and LSP. Anti-CD3 MoAb inhibited only this last cytotoxicity, suggesting that these clones showed NK-like activity. No clones showed LAK activity against Raji cell line.
ANITCARD10LIPINANflBzX KEslBlE~-mR-
BINDII'#STOPL4'IElET~~A INAUID~DISOWERS
NAlbamsht-am, ENHamis!@dl, IQ A Gil%I,P JJV&qos%DEndGRVM.&eslQFRCP.Ladcn(En@nd)and Ms&idY&).
197
in mist
(CS)
RESPONSE
IN
IDIOPATHIC
PRO-
R. Moscicki, M.D., H. Ramadan, M.D., 0. Castro, M.D., J. Nadol, M.D., K.J. Bloch, M.D., Boston,MA It has been suggested that SNHL may be immunologically mediated. We studied 21 patients with bilateral SNHL, progressive over days to months and without other identifiable etiology. Four patients had either juvenile rheumatoid arthritis systemic lupus erythematosis, polychondritis or poIymysitis. Blood lymphocytes from 17 patients and 10 controls were incubated with human cadaver cochlear and vestibular extracts; no consistent proliferative response was obtained. Circulating immune complexes (IC).were detected by Raji cell assay in 8 of 15 patients tested. Nine patients were treated with low doses of CS for 10 days or less; 7 responded but all relapsed when CS therapy was stopped. Nine patients received 60 mg prednisone daily for one month. If a beneficial result was obtained, the dose of CS was tapered over 2-3 months and treatment stopped. Eight patients responded to the high dose ,regimen. Two remained in remission for several years after treatment; 6 relapsed after a remission lasting 2-4 months. Nine of 10 patients given a second course of prednisone in high dosage responded and only two of these 9 relapsed on cessation of,treatment. Responders showed a mean improvement in speech reception threshold of 22+7dB. This study confirms the responsiveness of idyopathic, progressive SNHL to CS and suggests that 2 cycles of high dose CS therapy may induce longer remission than a single cycle or low dose treatment. We failed to find evidence of a specific cellular immune mechanism that might be the target for the CS effect.
ti'hQ
Recentstudiessl@gestthatemticardiolipinantibxlies @CA) sreassociatedwithrepeatedepiscdeeof~is,recur. Wniletheclinicda9 rentfeiallceeand~ scciationisstocmg,littleiskirsmoftinm&nisnwherebythe~ofACAresultsinthm&eis. nwzdm3ofthisstu~vieretodstexmine*thexp6A can b~plateletsinviiromritoi&ntifythe~tsof theplateletll&Xmme baRx3 by tkse anti~es. Wefandwpre-incut&i~ofAcApmitivesera with freeze-thm&plateletscarsedsignificart inhibiticnof aolti~~ipinactivi~inf~seratested.Anti~ffi withcs&iolipinbirdingsctivity!em-e suteeqmtly eluted ~lhessplatelets.Total~lipidextzectedfmn plezeletm&menee inhibitedcardiolipinbindingactivity. Separation of the extracted @r&olipid carpamnts by c&oma~suggestibatthetmgetem~srerhcephati~l serine,Ftxsphat~ltiitoland~ti$rle~lamine. we ccnclude that ACA canbti@r@rolipic?s ms&enesbutpmbebatialofthemmbreme occut-.
CORTICOSTEROID
GRESSIVE SENSORINEURAL HEARING LOSS (SNHL).
platelet fbxt
217
196
WITHDRAWN
LIVER-DERIVED T CELL CLONES IN AUTOIMMUNE CHRONIC ACTIVE HEPATITIS V. Barnaba, A. France, G. Ruberti, R. Benvenuto, C. Balsano, F. Balsano. Istituto I Clinica Medica, Universita "La Sapienza", Rome, Italy. 22 T cell clones expanded with PHA, rIL2 and irra diated autologous PBMC were generated by a liver derived T cell line recognizing autologous hepatE cytes expressing class II MHC antigens. 12 clones were CD3/CD8+ and 10 clones were CD3/CD4+. All clones resulted DR+ and TAC+ but none expressed CD16 or ~~11 molecules. 4 out of the CD8+ and 3 out of CD4+ T cell clones proliferated to autologous hepatocytes but not to irradiated autologous PBMC or HLA-DR+ allogeneic hepatocytes: anti-class II MoAb blocked the CD4+ clones proliferation against autologous hepatocytes as well as anti-class I MoAb blocked the CD8+ proliferation against autologous hepatocytes. All the CD8+ clones and 5 out of 10 CD4+ clones expressed CTL activity evaluated by lectin-Dependent-Cytotoxicity (LDCC). 10 out of 12 CD8+ clones and 3 out of 10 CD4+ clones showed NK activity against K562 cell line. 3 out of these10 CD8+ clones had cytotoxic activity against an human hepatocarcinoma cell line (PLC/PRF/5), producing HBsAg and LSP. Anti-CD3 MoAb inhibited only this last cytotoxicity, suggesting that these clones showed NK-like activity. No clones showed LAK activity against Raji cell line.
ANITCARD10LIPINANflBzX KEslBlE~-mR-
BINDII'#STOPL4'IElET~~A INAUID~DISOWERS
NAlbamsht-am, ENHamis!@dl, IQ A Gil%I,P JJV&qos%DEndGRVM.&eslQFRCP.Ladcn(En@nd)and Ms&idY&).
197
in mist
(CS)
RESPONSE
IN
IDIOPATHIC
PRO-
R. Moscicki, M.D., H. Ramadan, M.D., 0. Castro, M.D., J. Nadol, M.D., K.J. Bloch, M.D., Boston,MA It has been suggested that SNHL may be immunologically mediated. We studied 21 patients with bilateral SNHL, progressive over days to months and without other identifiable etiology. Four patients had either juvenile rheumatoid arthritis systemic lupus erythematosis, polychondritis or poIymysitis. Blood lymphocytes from 17 patients and 10 controls were incubated with human cadaver cochlear and vestibular extracts; no consistent proliferative response was obtained. Circulating immune complexes (IC).were detected by Raji cell assay in 8 of 15 patients tested. Nine patients were treated with low doses of CS for 10 days or less; 7 responded but all relapsed when CS therapy was stopped. Nine patients received 60 mg prednisone daily for one month. If a beneficial result was obtained, the dose of CS was tapered over 2-3 months and treatment stopped. Eight patients responded to the high dose ,regimen. Two remained in remission for several years after treatment; 6 relapsed after a remission lasting 2-4 months. Nine of 10 patients given a second course of prednisone in high dosage responded and only two of these 9 relapsed on cessation of,treatment. Responders showed a mean improvement in speech reception threshold of 22+7dB. This study confirms the responsiveness of idyopathic, progressive SNHL to CS and suggests that 2 cycles of high dose CS therapy may induce longer remission than a single cycle or low dose treatment. We failed to find evidence of a specific cellular immune mechanism that might be the target for the CS effect.
ti'hQ
Recentstudiessl@gestthatemticardiolipinantibxlies @CA) sreassociatedwithrepeatedepiscdeeof~is,recur. Wniletheclinicda9 rentfeiallceeand~ scciationisstocmg,littleiskirsmoftinm&nisnwherebythe~ofACAresultsinthm&eis. nwzdm3ofthisstu~vieretodstexmine*thexp6A can b~plateletsinviiromritoi&ntifythe~tsof theplateletll&Xmme baRx3 by tkse anti~es. Wefandwpre-incut&i~ofAcApmitivesera with freeze-thm&plateletscarsedsignificart inhibiticnof aolti~~ipinactivi~inf~seratested.Anti~ffi withcs&iolipinbirdingsctivity!em-e suteeqmtly eluted ~lhessplatelets.Total~lipidextzectedfmn plezeletm&menee inhibitedcardiolipinbindingactivity. Separation of the extracted @r&olipid carpamnts by c&oma~suggestibatthetmgetem~srerhcephati~l serine,Ftxsphat~ltiitoland~ti$rle~lamine. we ccnclude that ACA canbti@r@rolipic?s ms&enesbutpmbebatialofthemmbreme occut-.
CORTICOSTEROID
GRESSIVE SENSORINEURAL HEARING LOSS (SNHL).
platelet fbxt
217