Reference distributions for immunoglobulins A, G, and M: A comparison of a large cohort to the world's literature

Ritchie, Robert F.; Palomaki, Glenn E.; Neveux, Louis M.; Navolotskaia, Olga

doi:10.1002/(sici)1098-2825(1998)12:6<371::aid-jcla7>3.0.co;2-t

Cited by 30 publications

(27 citation statements)

References 87 publications

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“…[30][31][32][33][34] Black children and adults tend to have higher values than whites. [31][32][33] The results of the current study demonstrate that the black group has significantly higher circulating levels of complement proteins, C3 and C4, as well as immunoglobulin classes and subclasses, IgA, IgG1 and IgG3. IgG1 and IgG3 are strong activators of the classic pathway of complement, while IgA activates the alternative complement pathway.…”

Section: Discussionmentioning

confidence: 99%

Complement, immunoglobulin and creatine kinase response in black and white males after muscle-damaging exercise

McKune¹,

Semple

Smith

et al. 2009

S. Afr. j. sports med.

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Racial disparities have been demonstrated in athletic performance 1 and in the predisposition towards specific diseases.2 Immune/inflammatory pathways may be important in the pattern and/or progression of disease. 3,4 Research has demonstrated differences in the level of circulating immune/inflammatory markers as well as genotypic differences which may help to explain disease predisposition in specific racial groups. 3,4 In contrast, there is limited information relating to immune/inflammatory responses to exercise between racial groups. Such information is particularly relevant -strenuous exercise has been shown to alter immune/inflammatory responses predisposing athletes to infection and possibly injury, 5 which would ultimately impact on training and performance.Eccentric and/or strenuous unaccustomed exercise has been shown to elicit changes in skeletal muscle morphology.6 These changes are typically accompanied by increases in circulating creatine kinase (CK), local muscle swelling and soreness as well as alterations in circulating inflammatory markers such as leucocytes and cytokines. 7-9 Based on these observations, researchers have utilised exercise, particularly eccentrically biased exercise, to induce muscle damage and investigate immune/inflammatory sequelae.The key components of innate and adaptive immunity are the complement system and immunoglobulins, respectively. The complement system is composed of a number of proteins that are intricately involved in a variety of immune-related functions. Complement has been described as an important role player in cellular activation, chemotaxis, inflammation and clearance of immune complexes. [10][11][12] Immunoglobulins are crucial components of humoral immunity, having pathogen neutralisation and orIgInal research arTIcle complement, immunoglobulin and creatine kinase response in black and white males after muscle-damaging exercise abstract objectives. To determine the effect of eccentrically biased exercise and ethnic group on circulating levels of complement, immunoglobulin creatine kinase. Seven black and 8 white males (18 -22 years), active but untrained, participated in the study. Subjects performed a 60-minute downhill run on a treadmill (gradient -13.5%) at a speed eliciting 75% of their VO2 peak on a level grade. Venipunctures were performed before, immediately after and then at 3, 6, 9, 12, 24, 48, and 72 hours afterwards. Plasma creatine kinase (CK) activity, serum complement (C3, C4) and immunoglobulin (total IgG, IgG1, IgG2, IgG3, IgG4, IgA) concentrations were compared using a repeated measures ANOVA.results. There was an interaction (p=0.0055) and ethnic group effect (p<0.0001) for CK activity with consistently higher levels in the black group. CK increased over time after the run, peaking at 12 h for both groups. C3, C4, total IgG, IgG1, IgG3, and IgA were significantly higher (ethnic group effect, p<0.001), and IgG2 significantly lower (ethnic group effect, p<0.001) in the black group. Significantly higher resting concentrations of total IgG...

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Section: Discussionmentioning

confidence: 99%

Complement, immunoglobulin and creatine kinase response in black and white males after muscle-damaging exercise

McKune¹,

Semple

Smith

et al. 2009

S. Afr. j. sports med.

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“…Patients were required to have an IgG level below 7–8 g/l [2 SD below the mean, or more accurately, below the 97.5th percentile, as immunoglobulin levels are not normally distributed (34)], as well as impaired vaccine challenge responses or absent isohemagglutinins and other secondary causes of hypogammaglobulinemia were to be excluded. The criteria did not include the characteristic histological features of the disorder or clinical sequelae resulting from the immune system failure (ISF).…”

Section: Review Of the Esid/pagid (1999) Criteria For Cvidmentioning

confidence: 99%

Comparison of Diagnostic Criteria for Common Variable Immunodeficiency Disorder

et al. 2014

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Common variable immunodeficiency disorders (CVIDs) are the most frequent symptomatic primary immune deficiency condition in adults. The genetic basis for the condition is not known and no single clinical feature or laboratory test can establish the diagnosis; it has been a diagnosis of exclusion. In areas of uncertainty, diagnostic criteria can provide valuable clinical information. Here, we compare the revised European society of immune deficiencies (ESID) registry (2014) criteria with the diagnostic criteria of Ameratunga et al. (2013) and the original ESID/pan American group for immune deficiency (ESID/PAGID 1999) criteria. The ESID/PAGID (1999) criteria either require absent isohemagglutinins or impaired vaccine responses to establish the diagnosis in patients with primary hypogammaglobulinemia. Although commonly encountered, infective and autoimmune sequelae of CVID were not part of the original ESID/PAGID (1999) criteria. Also excluded were a series of characteristic laboratory and histological abnormalities, which are useful when making the diagnosis. The diagnostic criteria of Ameratunga et al. (2013) for CVID are based on these markers. The revised ESID registry (2014) criteria for CVID require the presence of symptoms as well as laboratory abnormalities to establish the diagnosis. Once validated, criteria for CVID will improve diagnostic precision and will result in more equitable and judicious use of intravenous or subcutaneous immunoglobulin therapy.

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“…Serum samples were stored in aliquots at Ϫ70°C until use. Levels of C3 in serum samples were determined as described below and were within normal levels in all volunteers (mean, 1.91 mg/ml; standard deviation [SD], 0.68 mg/ml; range, 1.18 to 2.88 mg/ml) (26). Mean levels of IgG and IgM in the same samples were also determined and were, respectively, 11.68 (Ϯ1.82) mg/ml and 1.35 (Ϯ0.64) mg/ml.…”

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confidence: 99%

CovR Regulates Streptococcus mutans Susceptibility To Complement Immunity and Survival in Blood

et al. 2016

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b Streptococcus mutans, a major pathogen of dental caries, may promote systemic infections after accessing the bloodstream from oral niches. In this study, we investigate pathways of complement immunity against S. mutans and show that the orphan regulator CovR (CovR Sm ) modulates susceptibility to complement opsonization and survival in blood. S. mutans blood isolates showed reduced susceptibility to C3b deposition compared to oral isolates. Reduced expression of covR Sm in blood strains was associated with increased transcription of CovR Sm -repressed genes required for S. mutans interactions with glucans (gbpC, gbpB, and epsC), sucrose-derived exopolysaccharides (EPS). Consistently, blood strains showed an increased capacity to bind glucan in vitro. Deletion of covR Sm in strain UA159 (UAcov) impaired C3b deposition and binding to serum IgG and C-reactive protein (CRP) as well as phagocytosis through C3b/iC3b receptors and killing by neutrophils. Opposite effects were observed in mutants of gbpC, epsC, or gtfBCD (required for glucan synthesis). C3b deposition on UA159 was abolished in C1q-depleted serum, implying that the classical pathway is essential for complement activation on S. mutans. Growth in sucrose-containing medium impaired the binding of C3b and IgG to UA159, UAcov, and blood isolates but had absent or reduced effects on C3b deposition in gtfBCD, gbpC, and epsC mutants. UAcov further showed increased ex vivo survival in human blood in an EPSdependent way. Consistently, reduced survival was observed for the gbpC and epsC mutants. Finally, UAcov showed an increased ability to cause bacteremia in a rat model. These results reveal that CovR Sm modulates systemic virulence by regulating functions affecting S. mutans susceptibility to complement opsonization.

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Reference distributions for immunoglobulins A, G, and M: A comparison of a large cohort to the world's literature

Cited by 30 publications

References 87 publications

Complement, immunoglobulin and creatine kinase response in black and white males after muscle-damaging exercise

Complement, immunoglobulin and creatine kinase response in black and white males after muscle-damaging exercise

Comparison of Diagnostic Criteria for Common Variable Immunodeficiency Disorder

CovR Regulates Streptococcus mutans Susceptibility To Complement Immunity and Survival in Blood

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