T activation

Ramasethu, Jayashree; Luban, Naomi L.C.

doi:10.1046/j.1365-2141.2001.02301.x

Cited by 41 publications

(49 citation statements)

References 44 publications

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“…The proposed mechanism of action involves exposure of the T-antigen in red cells and platelets, as well as the renal endothelium, by the neuraminidase produced by the pneumococci. This is supported by the demonstration of exposed T-antigen in renal glomeruli by fluorescein-labeled peanut lectin [18]. There is an increased incidence of mortality when HUS is associated with pneumococcal infection.…”

Section: Discussionmentioning

confidence: 96%

“…Removing the N-acetylneuraminic acid exposes the normally hidden Huebner-Thomsen-Freidenreich antigen (T-antigen), which can then react with anti-T IgM antibody normally present in adult plasma [13,14,15]. This antigen-antibody reaction, known as T-antigen activation (T-activation), occurs more frequently in infants and children [16,17,18,19]. The polyagglutination phenomenon associated with microbial enzymatic action is usually transient, clearing once the bacterial infection is controlled, and only rarely persisting for months [20].…”

Section: Introductionmentioning

confidence: 99%

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Pneumococcus-induced T-antigen activation in hemolytic uremic syndrome and anemia

Cochran

Panzarino

Maes

et al. 2004

Pediatric Nephrology

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The hemolytic uremic syndrome (HUS) is most commonly associated with Escherichia coli, but has been associated with other infections such as Streptococcus pneumoniae. Pneumococcus-induced HUS carries an increased risk of mortality and renal morbidity compared with E. coli-induced HUS. The pneumococcal organism produces an enzyme, which can expose an antigen (T-antigen) present on erythrocytes, platelets, and glomeruli. Antibodies to the T-antigen, normally found in human serum, bind the exposed T-antigen, and the resultant antigen-antibody reaction (T-activation) can lead to HUS and anemia. Clinicians need to be aware to request specific testing when pneumococcus-induced HUS/anemia is suspected, as current blood banking techniques do not routinely test for the presence of the T-antigen. Once this association is documented, washing all blood products and avoiding plasma products, if possible, is recommended. Plasmapheresis can be considered for the more critically ill patient. The incidence of pneumococcus-induced HUS may be increasing. We report six cases of pneumococcus-induced HUS/anemia presenting at our hospital.

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Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

Pneumococcus-induced T-antigen activation in hemolytic uremic syndrome and anemia

Cochran

Panzarino

Maes

et al. 2004

Pediatric Nephrology

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“…This antigen can then react with anti-T IgM antibody present in plasma [26, 27, 28]. Prior studies have shown that this T-antigen activation, and subsequent reaction with antibody, occurs more frequently in infants and children [29, 30]. …”

Section: Discussionmentioning

confidence: 99%

Management of streptococcal pneumoniaeinduced hemolytic uremic syndrome: a case report

Weintraub

Ahluwalia

Dogra

et al. 2014

CNCS

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Hemolytic uremic syndrome (HUS) secondary to Streptococcus pneumoniae infections (pHUS) has been well reported in the literature and accounts for roughly 5% of all the cases of HUS. However, this condition is likely under-diagnosed and the incidence is believed to be increasing. Given this increase in incidence of pHUS, it is important to have an understanding of the optimal means to manage the disease. We report a case of a 2-year-old male with pneumonia, acute kidney injury (AKI), microangiopathic hemolytic anemia (MAHA), and thrombocytopenia, diagnosed with pHUS and successfully treated with antibiotics, washed red blood cell (RBC) transfusions, plasma exchange (PE) with 5% albumin replacement, steroids, and hemodialysis. The response seen in our patient adds to the current literature and further supports the use of PE with albumin in patients with pHUS.

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“…Cleavage of sialic acid exposes the ThomsenFriedenreich (T) antigen (Thomsen 1927), which has been detected on erythrocytes, platelets and endothelium in pHUS (Klein et al 1977). The majority of individuals possess anti-T IgM (Ramasethu and Luban 2001), which are postulated to bind to T and initiate a cascade of events leading to TMA (Brandt et al 2002;Cabrera et al 1998;Copelovitch and Kaplan 2008). It is not clear whether anti-T cause pHUS since they are cold reactive, and at 37 • C cause neither red-cell agglutination nor complement activation (Crookston et al 2000;Klein et al 1977;Moores et al 1975;Novak et al 1983;Seges et al 1981;Williams et al 1989).…”

Section: Pathogenesis Of Phusmentioning

confidence: 98%

Is complement a culprit in infection-induced forms of haemolytic uraemic syndrome?

Johnson

Waters

2012

Immunobiology

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T activation

Cited by 41 publications

References 44 publications

Pneumococcus-induced T-antigen activation in hemolytic uremic syndrome and anemia

Pneumococcus-induced T-antigen activation in hemolytic uremic syndrome and anemia

Management of streptococcal pneumoniaeinduced hemolytic uremic syndrome: a case report

Is complement a culprit in infection-induced forms of haemolytic uraemic syndrome?

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