Increased IgM level

Abstract: Schizophrenia is characterized by an interrelated activation of the immune-inflammatory response system (IRS) and the compensatory immune-regulatory system (CIRS), which downregulates the IRS. Deficit schizophrenia is characterized by a deficit in IgM-mediated autoimmune responses to tryptophan catabolites. The presence and correlates of IgM isotype antibodies to oxidative-specific epitopes (OSEs), nitroso (NO), and nitro (NO2) adducts in schizophrenia remain unknown. This study measured IgM antibodies to malondialdehyde (MDA), azelaic acid, phosphatidylinositol, oleic acid, NO-tryptophan, NO-albumin, NO-cysteinyl, and NO2-tyrosine in a sample of 80 schizophrenia patients, divided into those with and those without deficit schizophrenia, and 38 healthy controls. Deficit schizophrenia was characterized by significantly lower IgM antibody levels to all OSEs as compared with non-deficit schizophrenia and controls. Lowered IgM antibodies to MDA coupled with increased IgM levels to NO-cysteinyl and NO2-tyrosine strongly predict deficit schizophrenia versus non-deficit schizophrenia with an area under the ROC curve of 0.913. A large part of the variance (21.2–42.2%) in the negative symptoms of schizophrenia and excitation is explained by IgM antibody titers to MDA (inversely) and NO-cysteinyl and/or NO2-tyrosine (both positively). Lower IgM antibodies to MDA are significantly associated with impairments in episodic memory including direct and delayed recall. These findings further indicate that deficit schizophrenia is a distinct phenotype of schizophrenia, which is characterized by lower natural IgM antibody levels to OSEs and relative increments in nitrosylation and nitration of proteins. It is concluded that deficits in natural IgM attenuate CIRS functions and that this impairment may drive negative symptoms and impairments in episodic memory and thus deficit schizophrenia.

Abstract: A 68-year-old woman developed a meningoencephalitis 18 days after a tick bite. IgG and IgM antibodies against tick-encephalitis virus were demonstrated, by enzyme-linked immunoabsorbent assay, in both serum and cerebrospinal fluid (csf). Lymphoplasmocytic pleocytosis was present in csf for over six weeks, as was an increased IgM level. Three weeks after the onset of neurological symptoms and clearing of the encephalitis there occurred multiple peripheral pareses in the left leg which were slow to regress. Retrospectively, IgM and IgG antibodies against Borrelia burgdorferi were demonstrated in deep-frozen serum and csf. Since IgG antibodies against Borrelia burgdorferi, locally synthesised in csf, could also be demonstrated, it must be assumed that the patient had a double infection. It is suggested that in confirmed cases of tick-encephalitis with an atypical course an additional infection with Borrelia should be considered, because if present the latter can be successfully treated with high doses of penicillin.

Abstract: In view of the reported association of insulin-dependent diabetes mellitus (IDDM) with viral infections, (non-) islet-specific immune changes, and partial immunodeficiencies, we used immunonephelometry to measure circulating levels of IgM, IgG, and IgA in a registry-based group of IDDM patients under age 40 years at clinical onset (n = 397) and in age-matched nondiabetic siblings (n = 316) and control subjects (n = 322). Overall, IgM and IgA concentrations were higher, and IgG concentrations lower, in patients than in control subjects or siblings (P < 0.001). In siblings, IgM concentrations were higher than in control subjects (P < 0.001). Using age-adjusted reference intervals, abnormal Ig concentrations were noted in 27% of the patients at onset versus only 10% of the siblings and 7% of the control subjects (P < 0.001). For onset between 20 and 40 years (n = 220), 30% of the patients presented either increased IgM levels (21%) or decreased IgG levels (11%). Both independent phenomena occurred regardless of diabetes-associated immune and genetic markers. In patients and siblings, IgM levels were positively correlated with pancreatic lipase activity. In diabetic children (0-9 years; n = 65), a subgroup presented increased IgA levels (15%) in association with the highest HLA DQ-linked genetic risk and elevated IgM levels. The changes in total Ig concentrations at onset were largely reversed under insulin therapy. They may reflect exposure to environmental triggers, such as viral infections, or to (relative) insulinopenia prior to clinical disease onset. Whatever their cause, different serum Ig levels exist in different age groups of recent-onset IDDM patients.

Abstract: Salivary immunoglobulins and albumin were analysed in smoking and non-smoking immunocompetent and immunodeficient individuals. Stimulated and unstimulated saliva were compared as between individuals with selective immunoglobulin A deficiency (IgAd), common variable immunodeficiency (CVI) and immunocompetent individuals. Immunocompetent smokers showed increased levels of sIgA in unstimulated saliva, when compared with non-smoking immunocompetent individuals. In stimulated saliva, the immunocompetent smokers showed decreased levels of IgG and IgM. IgAd smokers showed decreased levels of albumin in unstimulated saliva, when compared with non-smoking IgAd individuals. The non-smoking individuals with IgAd showed increased levels of IgM in both unstimulated and stimulated saliva, when compared with immunocompetent smokers. The non-smoking CVI individuals showed decreased levels of IgG, IgA and IgM in unstimulated and stimulated saliva, as expected, when compared with the same group of immunocompetent individuals. The decreased levels of albumin in unstimulated saliva in IgAd smokers and comparable to that of the IgG non-smoking IgAd individuals support the observation of locally produced immunoglobulins that protect the oral mucosa. Instead of sIgA, non-smoking immunodeficient individuals with IgAd compensate with increased IgM levels in stimulated saliva. The increased levels of sIgA in unstimulated saliva in immunocompetent smokers may be a reflection of the protection of the oral mucosa.