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Serum Titers (serum + titer)

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Medical Sciences100%

Selected Abstracts

Mycoplasma pneumoniae infection in a clinical setting

PEDIATRICS INTERNATIONAL, Issue 5 2008
Norlijah Othman
Abstract Background: Mycoplasma pneumoniae infection predominantly affects the respiratory tract, although the other organs may also be involved. Previous studies compared the clinical features of patients with M. pneumonia pneumonia to other pathogens and these studies were predominantly adult case series rather than involving children. The objectives of the present study were to compare the clinical features, laboratory, and radiographic findings in children seropositive for M. pneumoniae infection with children tested for suspected M. pneumoniae infection who were seronegative. Methods: Using a retrospective review of children who had complement fixation test (CFT) performed for suspected M. pneumoniae infection, children were classified as seropositive if the acute phase serum titer was ,64, or paired samples taken 2,4 weeks apart showed a fourfold or greater rise in serum titer. In contrast, a patient with an antibody titer <64 or with paired sera showing less than a fourfold rise in titer was considered seronegative. Results: One hundred and fifty-one children were included. Seventy-six children had serological evidence of M. pneumoniae infection and the remaining 75 were seronegative. Children with M. pneumoniae infection were more likely to have fever >6 days duration prior to admission, crackles on auscultation, radiographic consolidation and thrombocytosis at presentation. In addition, M. pneumoniae infection was associated with pneumonia whereas seronegative children were more likely to have upper respiratory tract infection or asthma. Conclusions: Certain clinical parameters could assist in gauging the likelihood of M. pneumoniae infection in children, and thus direct whether antibiotic treatment is needed. [source]

Neuromyelitis optica: Pathogenicity of patient immunoglobulin in vivo,

ANNALS OF NEUROLOGY, Issue 5 2009
Monika Bradl PhD
Objective Severe inflammation and astrocyte loss with profound demyelination in spinal cord and optic nerves are typical pathological features of neuromyelitis optica (NMO). A diagnostic hallmark of this disease is the presence of serum autoantibodies against the water channel aquaporin-4 (AQP-4) on astrocytes. Methods We induced acute T-cell,mediated experimental autoimmune encephalomyelitis in Lewis rats and confronted the animals with an additional application of immunoglobulins from AQP-4 antibody,positive and ,negative NMO patients, multiple sclerosis patients, and control subjects. Results The immunoglobulins from AQP-4 antibody,positive NMO patients are pathogenic. When they reach serum titers in experimental animals comparable with those seen in NMO patients, they augment clinical disease and induce lesions in the central nervous system that are similar in structure and distribution to those seen in NMO patients, consisting of AQP-4 and astrocyte loss, granulocytic infiltrates, T cells and activated macrophages/microglia cells, and an extensive immunoglobulin and complement deposition on astrocyte processes of the perivascular and superficial glia limitans. AQP-4 antibody containing NMO immunoglobulin injected into naïve rats, young rats with leaky blood,brain barrier, or after transfer of a nonencephalitogenic T-cell line did not induce disease or neuropathological alterations in the central nervous system. Absorption of NMO immunoglobulins with AQP-4,transfected cells, but not with mock-transfected control cells, reduced the AQP-4 antibody titers and was associated with a reduction of astrocyte pathology after transfer. Interpretation Human anti,AQP-4 antibodies are not only important in the diagnosis of NMO but also augment disease and induce NMO-like lesions in animals with T-cell,mediated brain inflammation. Ann Neurol 2009;66:630,643 [source]

A novel subpopulation of B-1 cells is enriched with autoreactivity in normal and lupus-prone mice

ARTHRITIS & RHEUMATISM, Issue 12 2009
Xuemei Zhong
Objective B-1 cells have long been suggested to play an important role in lupus. However, reports to date have been controversial regarding their pathogenic or protective roles in different animal models. We undertook this study to investigate a novel subpopulation of B-1 cells and its roles in murine lupus. Methods Lymphocyte phenotypes were assessed by flow cytometry. Autoantibody secretion was analyzed by enzyme-linked immunosorbent assay, autoantigen proteome array, and antinuclear antibody assay. Cell proliferation was measured by thymidine incorporation and 5,6-carboxyfluorescein succinimidyl ester dilution. B cell Ig isotype switching was measured by enzyme-linked immunospot assay. Results Anti,double-stranded DNA (anti-dsDNA) autoantibodies were preferentially secreted by a subpopulation of CD5+ B-1 cells that expressed programmed death ligand 2 (termed L2pB1 cells). A substantial proportion of hybridoma clones generated from L2pB1 cells reacted to dsDNA. Moreover, these clones were highly cross-reactive with other lupus-related autoantigens. L2pB1 cells were potent antigen-presenting cells and promoted Th17 cell differentiation in vitro. A dramatic increase of circulating L2pB1 cells in lupus-prone BXSB mice was correlated with elevated serum titers of anti-dsDNA antibodies. A significant number of L2pB1 cells preferentially switched to IgG1 and IgG2b when stimulated with interleukin-21. Conclusion Our findings identify a novel subpopulation of B-1 cells that is enriched for autoreactive specificities, undergoes isotype switch, manifests enhanced antigen presentation, promotes Th17 cell differentiation, and is preferentially associated with the development of lupus in a murine model. Together, these findings suggest that L2pB1 cells have the potential to initiate autoimmunity through serologic and T cell,mediated mechanisms. [source]

Role of CTA1R7K-COL-DD as a novel therapeutic mucosal tolerance,inducing vector for treatment of collagen-induced arthritis

ARTHRITIS & RHEUMATISM, Issue 6 2009
Annemarie Hasselberg
Objective To determine whether a cholera toxin,derived, novel immunomodulating fusion protein, CTA1R7K-COL-DD, carrying the class II major histocompatibility complex H-2q,restricted type II collagen peptide aa 259,274, can induce therapeutic tolerance and prevent collagen-induced arthritis (CIA) when administered intranasally in DBA/1 mice, and to assess whether ADP-ribosylation at the mucosal membranes exerts a regulatory function such that the outcome of tolerance or immune enhancement can be controlled. Methods DBA/1 mice with CIA were treated intranasally with CTA1R7K-COL-DD. The therapeutic effect was monitored for 46 days after the onset of disease. Clinical scoring of disease, histologic examination of inflammation, and bone erosion were assessed, and cytokine levels were determined in the serum or supernatants from splenocytes stimulated with recall antigen. Results The protective effect of CTA1R7K-COL-DD resulted in roughly 60% of the mice having no clinical signs or histologic evidence of disease after treatment, and those with CIA had significantly milder disease with less bone erosion. The protective status was associated with lower serum titers of IgG1, IgG2a, IgG2b, and IgG3 anticollagen and a substantial decrease in the production of interleukin-6 (IL-6), IL-17, and interferon-,, while levels of IL-10 were markedly up-regulated both in the serum and at the T cell level. Conclusion The enzymatically inactive mutant fusion protein CTA1R7K-COL-DD provided substantial therapeutic protection against CIA following intranasal administration. The mechanism behind the effect appears to be mediated by peptide-specific regulatory T cells induced by mucosal exposure to the peptide containing CTA1R7K-COL-DD vector. In addition, ADP-ribosylation at the mucosal membranes acts as a key regulator controlling mucosal tolerance or immunity. [source]