Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0021051 (
immunodeficiency
)
71,517
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Evidence is presented that a homeostatic mechanism exists that maintains a normal T-cell count, but is unresponsive to abnormalities in CD4+ T-cell count and CD8+ T-cell count. Specifically, we hypothesize that in all cases of T-cell loss, whether selective or not, both CD4+ T cells and CD8+ T cells will be produced until the absolute T-cell count returns to normal, even if this produces or exacerbates abnormalities in the absolute CD4+ T-cell count and absolute CD8+ T-cell count. This hypothesis implies that the selective loss of CD4+ T cells will induce the production of both CD4+ T cells and CD8+ T cells with the result that T-cell count will return to normal, but a persistent CD8+
T-cell lymphocytosis
and CD4+ T-cell lymphopenia will be produced. To test this hypothesis, we monitored T-cell reconstitution in mice selectively depleted of CD4+ T cells through treatment with a CD4-specific monoclonal antibody (mAb). Consistent with our hypothesis, the absolute peripheral blood T-cell count in treated mice returned to that of controls after approximately 4 months. However, the absolute CD8+ cell count became 163% of controls and the absolute CD4+ cell count remained less than 63% of controls. Our hypothesis may have implications regarding the pathogenesis and treatment of human
immunodeficiency
virus (HIV) infection. In particular, the hypothesis implies that the unresolved CD4+ T-cell lymphopenia seen in the first several years of HIV infection is the "natural" consequence of the interaction of a selective CD4+ T-cell depleting virus and a nonselective T-cell replacing homeostatic mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:T-cell homeostasis: implications in HIV infection . 843 79
Most cases of infectious mononucleosis (IM) are caused by Epstein-Barr virus (EBV). Other pathogens have been reported to cause heterophile-negative mononucleosis-like syndrome, including cytomegalovirus (CMV) and human
immunodeficiency
virus type-1 (HIV-1). Primary CMV infection is often asymptomatic in immunocompetent individuals. In this article, we describe a patient with prolonged fever and fatigue, who developed transient monoclonal CD8+
T-cell lymphocytosis
after primary CMV infection. Monoclonal gene rearrangement of T-cell receptor (TCR) beta locus was transiently detected in DNA from peripheral lymphocytes. Monoclonal rearrangement and atypical lymphocytosis disappeared after treatment with anti-viral agents. These observations imply that monoclonal expansion of T-cells could be a reactive phenomenon of primary CMV infection and TCR gene rearrangement is not specific for malignancy. Physicians should carefully follow patients with monoclonal expansion of CD8+ T-cells after CMV-IM in order to rule out T cell malignancy.
...
PMID:[Cytomegalovirus-associated infectious mononucleosis-like syndrome accompanied by transient monoclonal expansion of CD8+ T-cells]. 1991 80