Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004364 (autoimmune disease)
 24,845 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of relapsing type of neuromyelitis optica following influenza-like illness treated successfully with steroids and corticotrophin has been described. Raised gamma-globulin in CSF was suggestive of an autoimmune disorder. Inspite of six relapses in 8 years she has minimal neurological deficit.
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PMID:Neuromyelitis optica (relapsing type). 18 Mar 5

The BXSB mouse spontaneously develops an autoimmune disease that resembles human systemic lupus erythematosus (SLE). During their lifetime, male BXSB mice show an increasing monocytosis in the peripheral blood as opposed to their female littermates. This monocytosis is unique among autoimmune-prone mice. To test the hypothesis that alterations at the stem cell level may be responsible for this monocytosis, myeloid bone marrow precursor cells were examined in both male and female BXSB mice from 4 to 40 weeks of age. The number of M-CSF responding stem cells (CFU-M) and the number of GM-CSF responding stem cells (CFU-GM) were higher than in all other inbred mouse strains tested. In addition, male BXSB mice developed a progressive increase of CFU-M and CFU-GM in the bone marrow during their lifetime, which paralleled the peripheral blood monocytosis. The monocytosis in male BXSB mice is the result of a further expansion of the strain-specific high number of macrophage precursors by intrinsic factors, which may be attributed to the influence of the Yaa factor. The sex-specific expanded mononuclear phagocyte system may promote the autoimmune process and may be one reason for the dramatic course of murine SLE in male BXSB mice.
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PMID:Expanded macrophage precursor populations in BXSB mice: possible reason for the increasing monocytosis in male mice. 145 27

Two cases of Vogt-Koyanagi-Harada disease with rare neurological complications were reported, which are one case with vestibular and cerebellar ataxia, and one with multiple cranial nerve palsies. The first case, a 32-year-old man, was admitted to our ophthalmologic department because of visual impairment. Two weeks later, he complained of gait disturbance. Limb and truncal ataxia, vestibular dysfunction and perceptive deafness were observed. Ophthalmologic examination revealed typical findings of Vogt-Koyanagi-Harada disease. CSF showed elevated protein and mononuclear pleocytosis. After treatment with oral steroid therapy, vestibular and cerebellar ataxia, and visual impairment improved. The second case, a 22-years-old man, showed the VIIth, VIIIth, IXth, and Xth cranial nerve palsies with visual impairment, and he was diagnosed to have cranial nerve palsies associated with Vogt-Koyanagi-Harada disease. After steroid therapy, there was a marked clinical improvement. Vogt-Koyanagi-Harada disease is an autoimmune disease against the melanocytes and involving tissues containing melanocytes such as uvea, meningea, skin and inner ear, etc.. Neurological complications except for meningitis and perceptive deafness have been rarely reported in Japan. Related to the present cases, possible pathogenesis was discussed.
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PMID:[Each one case of Vogt-Koyanagi-Harada disease with vestibular and cerebellar ataxia, and multiple cranial nerve palsies]. 266 96

A case of chronic polyneuropathy associated with ulcerative colitis was reported. The patient was 57-year-old man who developed sensory disturbances and muscle weakness in four extremities along with the digestive symptoms of ulcerative colitis. Neurological examination revealed that sensory impairment in all modalities, muscular atrophy and weakness in the distal portions of all extremities and decreased or absent muscle stretch reflexes. Laboratory data included sedimentation rate 119mm/hour, CRP 4+, increased IgG and IgM. Lumbar puncture revealed normal CSF pressures, increased protein and IgG content with almost normal cell count. Nerve conduction velocity was delayed dominantly in sensory nerves. Sural nerve biopsy demonstrated degeneration of myelin sheath and decreased number of large fibers. Teased nerve study showed shortened internodal distances with myelin ovoids. These data together with the clinical course of this patient suggested that this peripheral neuropathy might be resulted from the common pathogenesis for ulcerative colitis which is considered as autoimmune disease.
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PMID:Chronic polyneuropathy and ulcerative colitis. 272 50

Guillain-Barre syndrome is known as one of the autoimmune disease, but the etiology, pathophysiology relating immune reaction, as well as the treatment are not established. It still causes physical handicap although its rate is low. The causes, clinical symptoms and outcome of 132 cases of Guillain-Barre syndrome have been analyzed. The patients' ages ranged from 4 months to 15 years. The antecedent events for 56.1% of the patients were known. These were upper respiratory tract infection, unexplained fever, vomiting, diarrhea, vaccination, measles, german measles, shigellosis, mumps, hepatitis, pertussis and surgery in order of frequency. The CSF protein level reached a maximum at 12.3 +/- 9.5 days. Steroids did not influence the outcome of this disease. More studies are necessary to conquer the disease.
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PMID:Guillain-Barre syndrome in Korean children. 274 76

Lymphoid adenohypophysitis is an autoimmune disorder. Eighteen percent of the multipartums are reported to have autoantibodies to pituitary tissues. The symptoms in lymphoid adenohypophysitis, such as hypopituitarism and sellar tumors, exhibit spontaneous remission. The pituitary is a feasible target organ in other autoimmune diseases of the endocrine system. Of these patients, 19/287 showed a positive immune reaction with pituitary tissue antigens. Our three female patients with sellar and suprasellar mass were clinically diagnosed as having lymphoid adenohypophysitis, because of the spontaneous regression of tumors, or presence of immunologically and endocrinologically abnormal findings. The first case was a 31-year-old woman who had amenorrhea and galactorrhea syndrome for two years after delivery of her second child. CT scan revealed a supraseller enhanced mass lesion. She had concomitant signs of recurrent meningeal irritations. The number of cells in the CSF increased, though the protein concentration increased only slightly. During a one-year close observation, the suprasellar mass spontaneously regressed. The second patient was a 66-year-old woman. In 1945, she underwent hysterectomy and oophorectomy for appendicitis followed by adnexitis. She was admitted because of episodes of headache, vomiting and visual field defect in 1983. CT scan also showed a contrast enhanced mass in the suprasellar region. She had two episodes of high fever. After the treatment with antibiotics and anti-inflammatory agents for 4 months, the tumor disappeared. The third case was a 20-year-old female. She had neither neurological nor endocrinological abnormality, except for attacks of vertigo, nausea and vomiting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Lymphoid adenohypophysitis, with special reference to 2 cases with sellar tumors spontaneously disappearing on the CT]. 377 4

We describe eosinophilic meningitis associated with ibuprofen therapy in a young woman who had no evidence of underlying illness. Discontinuation of ibuprofen was followed by prompt resolution of symptoms and disappearance of eosinophils from the CSF. Ibuprofen has been implicated previously in only five cases of aseptic meningitis--all in patients with an underlying autoimmune disease. No drug has been implicated previously as a cause of eosinophilic meningitis to our knowledge.
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PMID:Eosinophilic meningitis and ibuprofen therapy. 653 31

A patient with Felty's syndrome and rheumatoid arthritis was treated with recombinant granulocyte stimulating factor rhG-CSF (Neupogen) in view of severe neutropenia. He had a prompt rise in his neutrophil count and associated with this a severe flare of his arthritis and a skin rash. rhG-CSF was stopped, his neutrophil count fell rapidly and his symptoms resolved. rhG-CSF and the resulting rise in neutrophil count may be associated with flare of autoimmune disease in susceptible individuals.
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PMID:Felty's syndrome treated with rhG-CSF associated with flare of arthritis and skin rash. 754 May 27

Multiple sclerosis (MS), a putative autoimmune disease of unknown etiology, is characterized by CNS perivascular inflammation, foci of demyelination, and elevated intrathecal production of oligoclonal IgG's. T and B cells, macrophages, and microglia are all implicated in contributing to the initiation and perpetuation of the disease. In this brief review we discuss the possible role of T cells, B cells, macrophages, and microglia in contributing to the initiation and perpetuation of inflammation and demyelination in MS. Data from the rodent model of MS, experimental allergic encephalomyelitis (EAE) supporting a immunological basis for the pathology of MS is noted. This paper discusses recent data suggesting an interaction of the above-mentioned cells, as well as serum and CSF proteins including complement and anti-myelin/oligodendrocyte antibodies, in the pathogenesis of MS and EAE. Additionally, this review describes each cell type including the clinical and experimental evidence for their contribution to the immunologically mediated pathology of MS. Following the description of the role of individual cells, there is consideration of: the possible interaction of cells with the blood brain barrier (BBB) under normal and pathologic inflammatory conditions; the traffic of cells into the CNS in inflammation; and the role of antigen presentation within the CNS in the initiation, and perpetuation, of the CNS immune response. Finally, the review suggests a role for T cells in the initiation, amplification, and possibly the termination of CNS inflammatory events with particular attention paid to the pattern of T cell activation and T cell cytokine production.
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PMID:Immunology of multiple sclerosis. 774 93

The autologous mixed lymphocyte reaction (AMLR) involves the activation of T cells by autologous antigen presenting cells. Cells are generated during the course of the AMLR that have suppressive properties in vitro. In the present study we investigated the induction of CD8+ T cells in the AMLR with suppressive properties and the mechanism by which these cells downregulate in vitro proliferative responses. Purified CD8+ but not CD4+ T cells activated in the AMLR in conditioned medium inhibited proliferation of autologous T cells by anti-CD3 or PPD. Nonactivated CD8+ T cells did not suppress. The CD8+ T cells activated in the AMLR in the presence of conditioned medium (CD8+ Tact) were CD11b negative and were noncytotoxic. The inhibitory effect of CD8+ Tact cells was completely abrogated by anti-IFN-gamma antibody, but not by anti-IL-4, anti-IL-10, or anti-TGF-beta antibody. The induction of CD8+ Tact cells in the AMLR was blocked by anti-IL-2 or by anti-GM-CSF antibody and the combination of these two recombinant cytokines could support the induction of suppressive CD8+ Tact cells. CD8+ Tact cells were defective in patients with chronic progressive multiple sclerosis (MS) as compared to patients with relapsing-remitting MS or normal controls. Our studies provide a basis for understanding the mechanism of suppression by human CD8+ T cells in terms of specific cytokines, and demonstrate the potential importance of these cells in a human autoimmune disease as their function is defective in patients with progressive MS.
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PMID:Inhibition of T cell responses by activated human CD8+ T cells is mediated by interferon-gamma and is defective in chronic progressive multiple sclerosis. 776 10


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