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PubMed1999

Gene therapy for autoimmune demyelinating disease of the central nervous system.

Gene therapy is currently being explored as a new therapeutic treatment of autoimmune disease. The genetic modification of autoreactive memory T cells (T cell-mediated gene therapy) and autoimmune target tissue (target tissue gene therapy) to produce immunoregulatory cytokines offers a promising way to regulate autoimmunity. Furthermore, regenerative gene therapy offers the possibility of delivering growth factors to damaged autoimmune target tissue as a way of mediating repair. In the current review we discuss the different experimental models that are being used to test the efficacy of gene therapy in that treatment of autoimmune disease. We also discuss the importance of regulating transgene expression to ensure the therapeutic transgene products are delivered specifically to the autoimmune milieu in an antigen-inducible, non-constitutive manner.

Demyelinating Autoimmune Diseases, CNS↗

PubMed2002

Chemokines and proteinases in autoimmune diseases and cancer.

Chemotactic cytokines or chemokines form a family of proinflammatory proteins that are functionally linked to various classes of proteases, including matrix metalloproteinases (MMPs). Both families of molecules are key players in the migration of inflammatory cells in autoimmune diseases and in invasive cancers. For example, the chemokine interleukin-8 acts as a fast secretagogue of gelatinase B in granulocytes and is increased in the synovial fluid of arthritis patients and may locally recruit and activate neutrophils. The latter are the most abundant inflammatory cell type in the joints of patients with rheumatoid arthritis. In the case of the inflamed joint, the contribution of matrix remodeling enzymes in the breakdown of cartilage and bone is trivial. Gelatinase B (MMP-9) was documented in autoimmune diseases and cancer by immunohistochemistry with the use of monoclonal antibodies. Studies in rheumatoid arthritis and multiple sclerosis led us to postulate the "Remnant Epitopes Generate Autoimmunity" or REGA model for autoimmunity. This model is based on the pathophysiological role of three major classes of molecules involved in aspecific primary immune defense mechanisms: the cytokines, the chemokines and the proteases. The REGA model has proven to be useful for the development of disease treatment strategies. Particular cytokines are disease-limiting and may thus be used for the treatment of autoimmune disorders. Cytokines and chemokines that induce enzymes promote disease and may be antagonized. Along this line of research, we have recently identified natural and biosynthetic chemokine antagonists. Some of these have shown potent antiviral activity against human immunodeficiency virus. It is expected that these might also become useful in the treatment of autoimmune diseases and invasive cancers. A similar effect may be expected by the antagonization of damaging proteases or with the use of recombinant or synthetic enzyme inhibitors.

Autoimmune Diseases↗

PubMed2002

Mixed peripheral blood stem cell transplantation for autoimmune disease in BXSB/MpJ mice.

We examined whether mixed allogeneic transplantation with syngeneic plus allogeneic peripheral blood stem cells (PBSCs) is sufficient to interrupt autoimmune processes in BXSB mice and confer a potential therapeutic option for the treatment of patients with autoimmune diseases. Eight-week-old BXSB mice were lethally irradiated and reconstituted with BALB/c (H-2(d))+BXSB (H-2(b)) PBSCs, in which the number of injected allogeneic progenitor cells was 5 times that of syngeneic progenitor cells. The survival of mixed PBSC chimeras (BALB/c+BXSB-->BXSB) was 80% at the age of 48 weeks, whereas that of full chimeras (BALB/c-->BXSB) was 90%. Mixed PBSC transplantation (PBSCT) prevented the production of anti-DNA antibodies and the development of lupus nephritis in BXSB recipients and induced tolerance to both allogeneic and syngeneic antigens. Moreover, mixed chimeras exhibited immunological functions superior to fully allogeneic chimeras. On the other hand, increases in the number of BXSB PBSCs resulted in the transfer of lupus nephritis in BXSB+BALB/c-->BALB/c mice. Thus, the number of hematopoietic progenitor cells from normal mice proved critical to the prevention of autoimmune diseases. We propose that mixed allogeneic PBSCT for the interruption of the autoimmune process can be carried out by injecting increased numbers of allogeneic normal hematopoietic progenitor cells to prevent the relapse of autoimmune diseases, although it is necessary to decide upon a minimum dose of syngeneic PBSCs to achieve the desired beneficial effects on autoimmunity.

Animals↗

PubMed2002

[Bullous pemphigoid, primary biliary cirrhosis and vitiligo: a multiple autoimmune syndrome?].

Bullous pemphigoid is the most frequent autoimmune blistering skin disease. There have been few reports of an association with primary biliary cirrhosis and vitiligo. We report the simultaneous occurrence of bullous pemphigoid and primary biliary cirrhosis in an 86-year-old patient who also suffered from vitiligo. Multiple autoimmune syndrome, proposed by Humbert and Dupond, can be divided into three groups based on preferential associations of autoimmune disorders. The association of bullous pemphigoid, cirrhosis biliary primary and vitiligo has been reported three times in the literature. This association is probably not fortuitous and suggests a pathogenic relationship. This association is not typical of the multiple autoimmune syndrome as defined by Humbert and Dupond but the collection of such observations may contribute to revise the classification of autoimmune disease and provide a better understanding of the pathophysiological mechanisms of autoimmunity.

Adrenal Cortex Hormones↗

PubMed2002

Protein and peptide array analysis of autoimmune disease.

Molecular cloning, sequencing of the human genome, and other major advances in biomedical research have contributed substantially to our understanding of autoimmune disease. Nevertheless, to date, such advances have failed to reveal the etiology of or yield curative therapies for autoimmune disease. New approaches are needed. Proteomics, the large-scale study of expression and function of proteins that compose our tissues and mediate disease, represents a powerful and promising strategy. We developed protein and peptide arrays to profile autoantibody responses in autoimmune disease. Protein and peptide array analysis of autoimmune samples is revealing human and pathogen proteins involved in initiation and perpetuation of autoimmunity. Proteomic determination of autoantibody profiles can be utilized for diagnosis, prognostication, and guiding tolerizing therapy for autoimmune disease.

Antigens↗

PubMed2002

[Autoimmune polyendocrine syndrome (APS)].

As a complement to basic research, thorough clinical investigation of rare diseases may provide fundamental elements which improve our understanding of still obscure pathophysiologic mechanisms. This is the case with immunoendocrinopathy syndromes. Since Addison's pioneer observations in the 19th century, physicians have known that some individuals and their families may be affected by several spontaneous endocrine insufficiencies that are associated with autoimmune extra-endocrine processes. APS-I or APECED syndrome appears in children firstly affected by recurrent muco-cutaneous candidiasis and hypoparathyroidism, followed by adrenocortical insufficiency and by other autoimmune processes. APS-I is a monogenic disorder resulting from one mutation in the AIRE gene. The protein encoded by AIRE is a nuclear transcription factor the precise target of which is still not known. AIRE is mainly expressed by cells playing a crucial role in the establishment of central T cell self-tolerance (medullary epithelium, macrophages and dendritic cells of the thymus). APS-I must be considered in children affected with recurrent candidiasis without any sign of primary immune deficiency. Scientific investigation of the biological nuclear events controlled by AIRE has to be pursued. Undoubtedly, their deciphering will increase our knowledge of the mechanisms responsible for the establishment of central T cell self-tolerance and will open novel strategies for managing many autoimmune diseases. APS-II is a more common syndrome characterized by adrenocortical insufficiency spontaneously occurring in non tuberculous adults and associated with autoimmune thyroiditis and/or type 1 diabetes. Contrary to APS-I, APS-II is linked to genetic loci of the major histocompatibility complex. There is no adrenal insufficiency in APS-III which includes autoimmune thyroiditis, type 1 diabetes, and other autoimmune extra-endocrine processes (like pernicious anemia and vitiligo).

Adrenal Glands↗

PubMed1992

Tolerance mechanism in experimental ovarian and gastric autoimmune diseases.

Neonatal splenocytes, neonatal thymocytes, or phenotypically mature adult thymocytes, transferred from normal BALB/c mice to syngeneic athymic nu/nu (or SCID) mice, led to autoimmune oophoritis and autoimmune gastritis, with corresponding serum autoantibodies, in the recipients. The overall disease incidence was 73%; the pathology ranged from mild to severe, with complete loss of ovarian follicles and gastric parietal cells. CD4+ neonatal spleen cells and CD4+ CD8- adult thymocytes were required for autoimmune disease induction. Adult spleen cells did not elicit disease, but they prevented disease when co-transferred with neonatal spleen cells. However, in confirmation of an earlier report by Sakaguchi et al., (J. Exp. Med. 161:72, 1985), a subset of adult splenic T cells expressing a low level of CD5 molecules elicited similar autoimmune diseases. Thus, self-reactive T cells responsible for autoimmune disease of the stomach and ovary are not effectively deleted in the thymus, and they exist in the peripheral lymphoid organs of normal mice. We conclude that the functional expression of the self-reactive T cells is ontogenetically regulated; whereas T cells in the neonatal mice readily elicited autoimmune diseases in nu/nu recipients, regulatory cells may render self-reactive T cells in the normal adults unresponsive.

Animals↗

PubMed2003

Low fasting serum triglyceride level as a precocious marker of autoimmune disorders.

The authors recently reported the occurrence of low fasting serum triglyceride (TG) and high free fatty acid (FFA) levels in idiopathic pulmonary fibrosis. TG estimation in diverse groups of patients with autoimmune disease or hyperactive immune response confirmed the occurrence of a similar decrease of TG. In some patients, serum FFA level was also evaluated. TG value in lean and obese patients was compared with that in lean (n = 108) and obese (n = 208) control subjects without autoimmune disease. In patients affected by autoimmune chronic thyroiditis with enhanced concentration of antithyroglobulin antibodies and without thyroidal failure (n = 24), lean and obese patients had reduced TG (-69/%, P < .01 and -52%, P < .0001, respectively). Both lean and obese patients affected by chronic active B or C hepatitis (n = 26), with autoantibodies and without signs of hepatic insufficiency or cirrhosis, presented reduced TG (-57%, P < .01 and -61%, P < .001, respectively). A marked TG decrease (-73%, P < .001) was observed in the lean patients affected by lupus-like syndrome (n = 7). The lean and obese patients with systemic lupus erythematosus or rheumatoid arthritis (n = 11) showed TG decrease (-66%, P < .01 and -55%, P < .05, respectively). In patients affected by anamnestic allergy or atopic dermatitis/asthma (n = 66), both lean and obese, TGs were reduced (-67%, P < .0001 and -62%, P < .001, respectively). In isolated cases of diverse autoimmune diseases (scleroderma, APECED [autoimmune polyendocrinopathy, candidiasis, and ectodermal dystrophy], urticaria or urticarial vasculitis, Reiter or Sjogren syndromes, ulcerative colitis or Crohn's disease, multiple sclerosis or Guillain-Barré syndrome) (n = 14), decreased TG was also observed both in the lean and obese subjects (-59%, P < .01 and -57%, P < .01, respectively). Concerning FFA (n = 69), value in lean patients (n = 22) vs that in lean controls (n = 18) was increased (520 +/- 31 vs 299 +/- 30 mcEq/L, +74%, P < .001), whereas value in obese patients (n = 18) vs that in obese control subjects (n = 11) was decreased (542 +/- 34 vs 774 +/- 62, -30%, P < .01). This opposite behavior of FFA in lean and obese patients needs to be confirmed. Data in this study seem to indicate that low TG value may be a precocious marker of autoimmunity or immune system hyperreactivity.

Adult↗

PubMed1992

Autoimmune demyelination in transgenic E alpha d-positive A.CA mice. Comparison with E-negative A.CA mice.

A body of literature exists implicating the major histocompatibility complex class II E molecule in development of immune tolerance and/or immunosuppression. To define better the regulatory mechanisms underlying susceptibility to experimental autoimmune encephalomyelitis, an autoimmune condition displaying major histocompatibility complex-II dependence, disease was induced in transgenic mice expressing a major histocompatibility complex-II E alpha d-transgene. This was compared with experimental autoimmune encephalomyelitis induced in age-matched E-negative, non-transgenic mice of the same strain. The results showed that experimental autoimmune encephalomyelitis could be induced by adoptive transfer methodology in both transgenic and non-transgenic mice of the A.CA (H-2f) strain. Virtually no differences were observed between the two mouse types with regard to disease onset, course, and neuropathology. The main difference noted was within nonirradiated recipient subgroups where the nonirradiated transgenic A.CA mice demonstrated greater inflammation and demyelination than the nonirradiated, non-transgenic mice throughout the disease course. Thus, the results did not support the idea that the E molecule, per se, is involved in the induction of tolerance or immunosuppressive mechanisms protecting against autoimmunity. In addition, histologic changes in the central nervous system of the A.CA strain, both transgenic and non-transgenic, differed in several respects from the changes observed in other more commonly studied susceptible strains. In A.CA mice, polymorphonuclear cells were a more prominent component of the acute inflammatory infiltrate and in chronic disease, large aggregates of lipid-laden macrophages and cholesterol clefts were present within white matter lesions. The present approach, using genetic manipulation of the immune system, may have relevance to the study of disease mechanisms in other putative autoimmune demyelinating disorders such as multiple sclerosis.

Animals↗

PubMed1992

Autoimmune neutropenia in Sheboygan County, Wisconsin.

Autoimmune neutropenia is thought to be an uncommon disorder in adults. Over a 2-year period, however, autoimmune neutropenia was diagnosed in seven adults in a county with a population of approximately 105,000 people. The median age of the patients was 52 years old (range of 22 to 81 years), and five of the seven patients were women. All seven patients had at least one other symptom of autoimmune disease. Three patients had splenomegaly, three patients had positive direct antiglobulin tests, and two patients had immune thrombocytopenia. Antibodies reacting to neutrophils were detected by either granulocyte agglutination (GA) or granulocyte immunofluorescence (GIF) testing in five of the seven patients. Antibodies in four patients reacted with an 80 kd neutrophil membrane glycoprotein, and antibodies from two people reacted with a 60 kd membrane glycoprotein. Three patients were given treatment with splenectomy, which resulted in only transient improvement in the neutrophil counts. Serious infections occurred in only three patients over the 2 years of observation. In summary, autoimmune neutropenia in adults may occur more often than appreciated. Most cases of autoimmune neutropenia in adults appear to be associated with other autoimmune phenomena.

Adult↗

PubMed1992

[Idiopathic dilated cardiomyopathy: a persistent viral infection or an organ-specific autoimmune disease? The trial of 2 major pathogenetic hypotheses].

Aetiology and pathogenesis of idiopathic dilated cardiomyopathy (DCM) are uncertain. The two major pathogenetic hypotheses are: 1) autoimmunity; 2) persistent viral infection. Indirect evidence for virus association comes from the finding of raised titres of antibody to coxsackievirus in DCM, but infectious virus has never been isolated in myocardium from DCM patients. Bowles et al. using the slot-blotting technique reported that enteroviral RNA was commonly detectable in the myocardium of patients with myocarditis (53%) and with DCM (52%). Other groups using this as well as more refined hybridization techniques have failed to confirm such a high prevalence. Detection of enteroviral genomic RNA in cardiac tissue does not, however, imply active infection or pathogenicity. Thus the mechanisms of chronic myocardial damage in the absence of whole competent infectious virus remain uncertain. The other major pathogenetic hypothesis in DCM involves autoimmune mediated damage to myocytes. Circulating organ specific autoantibodies have been reported in a quarter of a group of patients with idiopathic DCM. This suggests that there may be autoimmune mechanisms operating at least in this subset of patients, but the exact relation of these antibodies to the pathogenesis and prognosis needs to be defined. The abnormal expression of major histocompatibility complex class II antigens on cardiac microvascular endothelium in endomyocardial biopsy tissue from DCM patients, and the reported association with HLA-DR4 phenotype lend further support to the autoimmune hypothesis. The viral and the autoimmune hypothesis in chronic myocarditis and in DCM are not mutually exclusive. In experimentally murine virus-induced myocarditis infectious virus can no longer be recovered from the myocardium after two weeks, although nucleic acid sequences of the viral genome are still detectable. The development of chronic inflammation takes place only in mice with a predisposing genetic background. Chronic myocyte damage is associated with the production of circulating heart-specific autoantibodies and autoreactive lymphocytes. In this animal model chronic myocarditis appears to be a virus-triggered or precipitated autoimmune disease, rather than a persistent viral infection with tissue damage due to active virus synthesis and replication. A similar transition from acute myocarditis into DCM may occur in man.

Animals↗

PubMedDate not supplied

High efficacy of Rituximab in indolent HCV-related lymphoproliferative disorders associated with systemic autoimmune diseases.

OBJECTIVE: The evidence of an increased frequency of B-non Hodgkin's lymphomas (NHL) in patients with HCV and systemic autoimmune diseases suggests a close relationship between infection, autoimmunity and cancer. Choosing the best therapy for patients affected either by HCV-related lymphoma or autoimmune disorders is not easy; in fact, some treatments may be accompanied by an excessive hepatic toxicity and may be followed by a reactivation of hepatitis. There is growing interest in the search for an ideal therapy for this kind of patient. Thanks to its mechanism of action and good toxicity profile, Rituximab could prove to be an attractive therapeutic option: it has been reported to be highly active in low-grade NHLs and has been proposed for the management of autoimmune diseases. RESULTS: In this paper we evaluate the role of anti-CD20 monoclonal antibody in mono-therapy in 10 patients with either indolent HCV-related lymphoma or autoimmune disease. A very high rate of response, of both NHL and of the associated autoimmune disease, was observed (100% of clinical response), with no significant hepatic and extra-hepatic toxicity. CONCLUSION: Thus, although the number of patients was small, our data strongly support the use of anti-CD20 in this patient setting.

Adult↗

PubMed2006

Pulmonary arterial hypertension in autoimmune diseases: an analysis of 19 cases from a medical center in northern Taiwan.

BACKGROUND AND PURPOSE: Pulmonary arterial hypertension (PAH), a serious complication of autoimmune diseases, has rarely been reported in Taiwan. METHODS: Nineteen patients with various autoimmune diseases diagnosed with PAH at Taipei Veterans General Hospital from 2002 to 2004 were enrolled; the underlying autoimmune diseases included systemic lupus erythematosus (n = 6), primary Sjögren's syndrome (n = 5), systemic sclerosis (n = 4), adult-onset Still's disease (n = 2), and mixed connective tissue disease (n = 2). The characteristic manifestations of underlying autoimmune diseases and the clinical features of PAH were analyzed. RESULTS: There were 16 female and 3 male patients. The median age at onset of PAH was 44 years and the mean right ventricular systolic pressure (RVSP) was 67.9 mm Hg. Patients without pneumonitis had a significantly higher RVSP value than those with pneumonitis (77.5 +/- 24.3 vs 54.8 +/- 18.4 mm Hg, p=0.041). Four out of 7 patients (57.1%) with RVSP >or=80 mm Hg and 1 out of 12 patients (8.3%) with RVSP <80 mm Hg died. In all of the 19 patients, the severity of RVSP was significantly correlated with serum uric acid (UA) level (r = 0.686, p=0.001). Among the PAH patients without pneumonitis, the severity of RVSP inversely correlated with the diffusion capacity of the lung for carbon monoxide (DLCO) [r = -0.856, p=0.003]. The characteristic manifestations of underlying autoimmune diseases included a high incidence of Raynaud's phenomenon (15/19, 78.9%), a high titer of antinuclear antibody (13/17, 76.5%), positive anti-ribonucleoprotein antibody (8/15, 53.3%), hypergammaglobulinemia (15/19, 78.9%), hyperuricemia (13/19, 68.4%), and less renal involvement. CONCLUSIONS: PAH in autoimmune diseases could be potentially fatal with characteristic manifestations. Moreover, RVSP correlated directly with serum UA level and inversely with DLCO.

Adult↗

PubMed1991

Three theories which explain the occurrence and inheritance of the autoimmune diseases.

The immunity system uses random processes. In B lymphocytes these are antigen-driven somatic gene mutations which tighten antibody affinity for invading microbes to enable recovery from and prevention of infectious diseases. In T lymphocytes, randomized gene segment combinations continually provide new clones, needed to counter continually-changing microbial parasites. Because these B and T cell processes are random, they entail risk of producing forbidden (self-antigen-reactive) clones, a minority of which cause autoimmune diseases, as envisaged by Burnet in his forbidden clone theory. A corollary of the forbidden clone theory is the V gene theory, postulating that the specificities of the germline variable (V) genes coding for antigen receptors influence the risks of autoimmune diseases. The H gene theory, postulates that the main defense against autoimmune disease is mediated by the permanent, unbreakable tolerances imposed on the clonal repertoire by the histocompatibility (H) antigens, major, minor and H-Y. Recent work shows that the last two act as peptides which modify MHC antigens by occupying their Bjorkman grooves. The absolute absence of autoimmunity to histocompatibility, ABO and H-Y antigens shows that nascent clones with high affinity for these white cell antigens are continually eliminated. Application of molecular biological techniques has shown that H antigen tolerance impositions profoundly alter the clonal repertoire and hence the risks of development of the forbidden clones which cause the autoimmune diseases. Precise basic theory is crucially important for effective application of molecular biology and microbiology to the eminently achievable therapeutic and prophylactic conquest of the ubiquitous autoimmune diseases.

Animals↗

PubMed2007

[Autoimmune hepatitis in children].

BACKGROUND: Autoimmune mechanisms are involved in the pathogenesis of autoimmune hepatitis and primary sclerosing cholangitis. The disorders are rare but important to diagnose, as immunomodulating therapy can prevent liver failure. Cases of "overlap syndrome" between autoimmune hepatitis and primary sclerosing cholangitis are described. MATERIAL AND METHODS: We have studied the medical records of children diagnosed with hepatitis and cholangitis treated at Rikshospitalet University Hospital from 1986 through 2004. Symptoms, findings and disease course are presented. A general overview is given of autoimmune hepatitis, primary sclerosing cholangitis and overlap syndrome in children. RESULTS: 18 children were identified; 11 with autoimmune hepatitis, six with primary sclerosing cholangitis and one with overlap syndrome. Four of the children with primary sclerosing cholangitis had inflammatory bowel disease; two of them had ulcerative colitis and two had Crohn's disease. The patient with overlap syndrome had ulcerative colitis. Pathology was found in the liver biopsies of all the children. Sixteen patients were treated with prednisolone and azathioprine. Most of the children responded to immunomodulating therapy with normalization of liver function tests. Many relapsed while tapering steroids. None of the patients have needed a liver transplant. CONCLUSION: It is important to diagnose children with autoimmune liver disease, as children tend to respond well to immunomodulating therapy.

Adolescent↗

PubMed1990

[Autoimmune polyglandular syndrome. Clinical experience in 21 cases].

The autoimmune polyglandular syndrome is characterized by the association of 2 or more endocrine disorders of autoimmune origin which may coexist with autoimmune disorders in other organs. Roughly 25% of patients with an autoimmune endocrinopathy show evidence of autoimmune disease elsewhere. We report 21 patients with autoimmune polyglandular syndrome classified according to Neufeld.

Adult↗

PubMed1990

Analysis of B-cell abnormalities in autoimmune mice by in vitro culture system using two types of bone marrow stromal cell clone.

B-cell abnormalities in 4-week-old autoimmune NZB and NZB/WF1 mice were studied with an in vitro culture system using two types of stromal cell clone, ST2 and PA6. ST2 supports B lymphopoiesis, and PA6 maintains B progenitors which do not express a B-lineage antigen (B220), but does not allow their further differentiation into B220+ B-lineage cells. B progenitors developed into B-lineage cells when transferred to the ST2 layer. B-lineage cells generated in this way showed hyperproliferation autoimmune mice, and the frequencies of B-lineage cells in the bone marrow of these mice were high. In contrast, the frequencies of B progenitors in the bone marrow were low. These results suggest that abnormal B-cell formation in autoimmune bone marrow appears at a very early stage of B-cell differentiation, and that B-lineage cells are hyperactive on the ST2 layer in the absence of microenvironmental elements from autoimmune bone marrow. This study indicates that autoimmune B-cell abnormalities can be reproduced in vitro, giving new data at the level of committed B progenitors, suggesting that this culture system will be a useful tool for investigating haemopoietic stem-cell abnormalities in autoimmune mice.

Animals↗

PubMed1989

Cystic ovarian enlargement resulting from autoimmune oophoritis.

Autoimmune oophoritis is a rare cause of premature ovarian failure. Previous studies of autoimmune oophoritis have detailed the clinical, immunologic, and histologic findings. The gross pathologic features of the involved ovaries have detailed the clinical, immunologic, and histologic findings. The gross pathologic features of the involved ovaries have not been emphasized. Herein, we describe a 35-year-old woman with autoimmune oophoritis who presented with symptoms referable to a right cystic adnexal mass. She underwent a diagnostic laparotomy and right salpingo-oophorectomy for removal of an 8.0-cm-diameter, twisted multicystic ovary. Microscopically, mononuclear inflammatory cells infiltrated multiple follicular and luteal cysts. We have seen two additional patients with histologically verified autoimmune oophoritis who underwent diagnostic laparotomy and oophorectomy because of cystic enlargement of the ovaries. Stimulation of ovarian follicles by elevated levels of pituitary gonadotropins probably causes the cystic changes. Recognition of this aspect of autoimmune oophoritis may help to prevent oophorectomy in patients whose functioning ovarian tissue is already compromised by autoimmune destruction.

Adult↗