Search results
Results from the WOW.Com Content Network
Antiretroviral therapy, the most common treatment for patients with HIV, has been shown to restore CD4+ T cell counts. [20] The body responds to T cell depletion by producing an equal amount of T cells. However, over time, an individual's immune system can no longer continue to replace CD4+ T cells. [21] This is called the "tap and drain ...
White fat cells contain a single large lipid droplet surrounded by a layer of cytoplasm, and are known as unilocular. The nucleus is flattened and pushed to the periphery. A typical fat cell is 0.1 mm in diameter [2] with some being twice that size, and others half that size.
Neither DGAT1 nor DGAT2 is singularly essential for TAG synthesis or droplet formation, though mammalian cells lacking both cannot form lipid droplets and have severely stunted TAG synthesis. DGAT1, which seems to prefer exogenous fatty acid substrates, is not essential for life; DGAT2, which seems to prefer endogenously synthesized fatty acids ...
A lipid storage disorder (or lipidosis) is any one of a group of inherited metabolic disorders in which harmful amounts of fats or lipids accumulate in some body cells and tissues. [1] People with these disorders either do not produce enough of one of the enzymes needed to metabolize and break down lipids or, they produce enzymes that do not ...
Now, having lipid deposits in the white blood cells of the individual is known and recognized as Jordans' anomaly, due to the medical professional who discovered it. [10] The first case of neutral lipid storage disease was reported by Maurice Dorfman when he treated two sisters with non-bullous ichthyosiform erythroderma in 1974. [2]
Sézary disease, or Sézary syndrome, [1] is a type of cutaneous T-cell lymphoma that was first described by Albert Sézary. [2] The affected T cells, known as Sézary's cells or Lutzner cells, have pathological quantities of mucopolysaccharides. Sézary disease is sometimes considered a late stage of mycosis fungoides with lymphadenopathy. [3] [4]
It acts as a negative regulator of T-cell activation. Mutation in this gene is a risk factor for many autoimmune diseases. Weaker T-cell signaling may lead to impaired thymic deletion of autoreactive T cells, and increased PTPN22 function may result in inhibition of regulatory T cells, which protect against autoimmunity. [35]
T cell exhaustion can be triggered by several factors like persistent antigen exposure and lack of CD4 T cell help. [64] Antigen exposure also has effect on the course of exhaustion because longer exposure time and higher viral load increases the severity of T cell exhaustion. At least 2–4 weeks exposure is needed to establish exhaustion. [65]