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Administration of interleukin-7 increases CD4 T cells in idiopathic CD4 lymphocytopenia.
- Source :
-
Blood . 2/25/2016, Vol. 127 Issue 8, p977-988. 12p. - Publication Year :
- 2016
-
Abstract
- Idiopathic CD4 lymphopenia (ICL) is a rare syndrome defined by low CD4 T-cell counts (<300/mL) without evidence of HIV infection or other known cause of immunodeficiency. ICL confers an increased risk of opportunistic infections and has no established treatment. Interleukin-7 (IL-7) is fundamental for thymopoiesis, T-cell homeostasis, and survival of mature T cells, which provides a rationale for its potential use as an immunotherapeutic agent for ICL. We performed an open-label phase 1/2A doseescalation trial of 3 subcutaneous doses of recombinant human IL-7 (rhIL-7) per week in patients with ICL who were at risk of disease progression. The primary objectives of the study were to assess safety and the immunomodulatory effects of rhIL-7 in ICL patients. Injection site reactions were the most frequently reported adverse events. One patient experienced a hypersensitivity reaction and developed non-neutralizing anti-IL-7 antibodies. Patients with autoimmune diseases that required systemic therapy at screening were excluded from the study; however, 1 participant developed systemic lupus erythematosus while on study and was excluded from further rhIL-7 dosing. Quantitatively, rhIL-7 led to an increase in the number of circulating CD4 and CD8 T cells and tissue-resident CD3 T cells in the gut mucosa and bone marrow. Functionally, these T cells were capable of producing cytokines after mitogenic stimulation. rhIL-7 was well tolerated at biologically active doses andmay represent a promising therapeutic intervention in ICL. This trial was registered at www.clinicaltrials.gov as #NCT00839436. [ABSTRACT FROM AUTHOR]
- Subjects :
- *LYMPHOPENIA
*IMMUNODEFICIENCY
*INTERLEUKIN-1
*HOMEOSTASIS
*ALLERGIES
Subjects
Details
- Language :
- English
- ISSN :
- 00064971
- Volume :
- 127
- Issue :
- 8
- Database :
- Academic Search Index
- Journal :
- Blood
- Publication Type :
- Academic Journal
- Accession number :
- 113323885
- Full Text :
- https://doi.org/10.1182/blood-2015-05-645077