Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P14784 (IL-2 receptor)
 3,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Both severe combined immunodeficiency (SCID) and cystic fibrosis (CF) may present in infancy with a history of respiratory infections and failure to thrive. Elevated sweat chloride levels on multiple sweat tests is diagnostic of CF; transient elevation of sweat chloride has been reported in patients with hypogammaglobulinemia and antibody deficiency without CF. This article presents a case report of a 5-month-old boy with recurrent respiratory infections, failure to thrive, and two borderline elevated sweat test levels. Laboratory evaluation including testing for CF as well as immune deficiency was performed in this patient. Two borderline abnormal sweat chloride tests together with isolation of Pseudomonas from the airway caused clinicians initially to suspect CF; however, mutation in gene coding for the gamma-chain of the IL-2 receptor and a negative CF genetic mutation analysis ultimately led to the final diagnosis of SCID. It is essential to make the diagnosis of SCID as early as possible because infants with SCID who do not undergo reconstitution of their immune system universally die in infancy because of infection. Early diagnosis and intervention can lead to an excellent prognosis in a previously fatal disease.
Allergy Asthma Proc
PMID:A 5-month-old boy with recurrent respiratory infections, failure to thrive, and borderline elevated sweat chloride levels. 1691 75

TNF receptor superfamily member 25 (TNFRSF25; also known as DR3, and referred to herein as TNFR25) is constitutively and highly expressed by CD4(+)FoxP3(+) Tregs. However, its function on these cells has not been determined. Here we used a TNFR25-specific agonistic monoclonal antibody, 4C12, to study the effects of TNFR25 signaling on Tregs in vivo in mice. Signaling through TNFR25 induced rapid and selective expansion of preexisting Tregs in vivo such that they became 30%-35% of all CD4(+) T cells in the peripheral blood within 4 days. TNFR25-induced Treg proliferation was dependent upon TCR engagement with MHC class II, IL-2 receptor, and Akt signaling, but not upon costimulation by CD80 or CD86; it was unaffected by rapamycin. TNFR25-expanded Tregs remained highly suppressive ex vivo, and Tregs expanded by TNFR25 in vivo were protective against allergic lung inflammation, a mouse model for asthma, by reversing the ratio of effector T cells to Tregs in the lung, suppressing IL-13 and Th2 cytokine production, and blocking eosinophil exudation into bronchoalveolar fluid. Our studies define what we believe to be a novel mechanism for Treg control and important functions for TNFR25 in regulating autoaggression that balance its known role in enhancing autoimmunity.
 ...
PMID:Therapeutic Treg expansion in mice by TNFRSF25 prevents allergic lung inflammation. 2128 18


<< Previous 1 2 3