Heavy applications of suspensions of killed Malassezia ovalis on rabbit skin produced lesions that both grossly and microscopically resembled human psoriasis. This system may afford not only a model but also an explanation for that disease.
Activation of C3 and factor B in normal human serum by P. ovale was demonstrated using a standard unidirectional immunoelectrophoresis technique. Activation of complement by the alternative (properdin) pathway is a possible mechanism by which P. ovale may mediate an inflammatory response.
, S y r a c u s e , .~~ The complement system of twenty-four patients with psoriasis was studied in detail. Quantitation of classical pathway components (C4, C3, C3-C9) and the a b i l i t y of the patient's serum to support lysis of antibody-coated target cells and C3-C9 consumption a f t e r incubation with a preformed immune precipitate were either normal or elevated. Alternative pathway evaluation involved quantitation of serum levels of factor B and properdin by radial immunodiffusion; in addition, the ability of the patient's serum to support C3-C9 activation with zymosan and cobra venom factor as well as lysis of unsensitized rabbit erythrocytes was also ascertained. Rabbit CH50 t i t e r s and factor B levels were normal or elevated in 23/24 and 24/24 patients respectively. Abnormally low properdin levels more than 2 standard deviations below the normal mean were seen in 14/24 patients. Mean C3-C9 consumption a f t e r zymosan or cobra venom factor incubation was significantly less than normal (p < .001 and 0.025); in 11/24 sera incubated with zymosan, the extent of C3-C9 activation was more than 2 S.D. below the normal mean. Thus, abnormalities of the complement system are clearly present in patients with psoriasis and seem limited to the alternative pathway. Further, these abnormalities suggest that this pathway may be involved in the genesis of this disorder. Children with clinically inactive SLE and JDMS may have abnormal immune function reflecting underlying defects. ADCC, mediated by Fc receptor bearing c e l l s , may play a role in these diseases by eliminating autoantibody coated cells; it i s abnormal in some adult SLE patients. ADCC and i t s inhibition by prednisolone have not been studied i n children with SLE or JDMS. W e have shown that ADCC i s inhibited by i n vitro prednisolone in healthy adults; the purpose of this study i s to determine if ADCC mediated by peripheral mononuclear c e l l s from children with SLE and JDMS i s inhibited by prednisolone. Chang c e l l s labelled with 51-chromium were used as targets. Neither 100 nor 50 ug/dl prednisolone significantly.decreased ADCC ( 7 2 . w 8 . 8 a t 64:l effector:target (E:T) ratio). 6 of these children had clinically inactive disease. 6 SLE patients studied showed a correlation of ADCC with t o t a l hemolytic complement (r=.62). There was no significant decrease i n ADCC when prednisolone was added to c e l l s from 4 children with DMS (70.354.3 a t 64:l E:T), only 1 of whom had active disease. It is concluded that i n vitro prednisolone inhibits ADCC from normal adults but not 7 of 9 children with SLE or 4 children with DMS. It i s speculated that lack of ADCC response to in vitro prednisolone may reflect altered c e l l subpopulations in children with inactive and active SLE and JDMS. (PMN) incubated with live INF-V consume oxygen, generate superoxide and produce chemiluminescence ( C L ) in the absence of serum. PMN exposed to virus incubated in 10% heated pre-immune human sera (PRE sera), in heated post immune sera (POST sera)...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.