By Univ.-Doz. Dr. Josef S. Smolen, Univ.-Doz. Dr. Christoph C. Zielinski (auth.)
More than a hundred and forty years in the past, lupus erythematosus (LE) was once famous as a sickness entity by means of clinicians operating within the box of dermatology, which had only in the near past turn into an self sufficient scientific self-discipline. quickly after cutaneous lupus used to be first mentioned, it used to be discovered that, except the surface, the disorder may contain different organs and hence be systemic in nature. The latter observations have been first made by way of MORITZ KApOSI , whose paintings has attracted renewed realization re cently and who succeeded FERDINAND VON HEBRA to the chair of dermatology on the scientific college in Vienna. The early description of lupus erythematosus in either its cutaneous and systemic manifes tations used to be therefore in detail linked to Vienna and its scientific tuition. the following part within the examine of lupus used to be characterised by way of an in crease in wisdom of the sort and volume of organ involvement. The paintings by way of OSLER , LIBMANN and SACKS , and KLEMPERER  most sensible represents those advances. the rise in scientific wisdom of LE eventually resulted in DUBOIS' well-known monograph , which used to be pub lished at a time of renewed curiosity in SLE, elicited by means of the descrip tion by way of HARGRAVES et al.  of the LE-cell phenomenon. A extra specified research of this discovering published that the ailment was once charac terized via an irregular immune reaction, even supposing its pathogenetic implications have been nonetheless unclear.
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Additional resources for Systemic Lupus Erythematosus: Clinical and Experimental Aspects
Impaired tolerance to heterologous gamma globulins characteristic of BXSB males [62, 63] is also dependent upon stem cells in the males . However, recent studies of (NZW x BXSB)FJ female mice show disease without a tolerance defect . The xid gene can suppress the acceleration due to the BXSB Y chromosome in BXSB mice and in (NZB x BXSB)FJ mice . This is consistent with studies suggesting that abnormal B cells in BXSB males are critical for disease expression [6163, 65, 66] and that such B cells do not develop in xid mice [65, 67, 68].
Moreover, the possibility of different genetic bases leaves open the possibility that somewhat different pathways to illness exist. If so, different approaches to therapy might be indicated in the different situations. Finally, attempts at prevention or prophylaxis would depend upon a fundamental understanding of the molecular genetic basis of disease. Quite different approaches to patient populations would be dictated by more than one genetic mechanism. As a result, the murine genetic studies should point the way to new approaches to the human condition.
Other approaches will be needed to unravel the complex genetic mechanisms underlying the autoimmune process. The evolution of new molecular technology, such as RNA subtraction, may allow the isolation of autoimmunity genes. Although this is an extremely difficult task at present, the success of recent efforts to isolate the T cell receptor genes [127-129] is encouraging. Genetic Aspects of Murine Lupus 39 Table 5. xid PLN NO NO NO ++++ ++++ + NO + NO + 0 0 0 0 ++ + ± ± + + (NZB X BXSB)FJ SP male (NZB x BXSB)FJ PLN male (NZB X BXSB)FJ SP female NO NO NO + + ± ± +++ ± ++ ++ NO C3H/HeJ SP C3H/HeJ PLN C3H/HeJ-g/d/g/d SP C3H/HeJ-g/d/g/d PLN ++ + ++ ++++ +++ +++ ++ ± +++ ++ NO NO NO NO ++ ++ + ± + + + ± + +++ ++ ++ + ± ++ + NO ± NO +++ NO NO NO NO NO NO CBA/J Spb CBAlJTHY OBAl2 THY MRL-+I+ THY MRL-pr//pr THY BXSB THY male NZB THY female " Summary of data on the expression of four oncogenes in different lymphoid organs of various autoimmune and control mouse strains.