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--- home:diseases:hiv_and_aids [02.17.2019] – [CD38] sallieq
+++ home:diseases:hiv_and_aids [02.19.2019] – [More research into CD38 and immune function] sallieq
@@ Line 37: / Line 37: @@
 Pathogens are able spread effectively in an immunocompromised environment. This means it's possible that AIDS patients pick up substantial pathogen loads. It is further possible that it is these Th1 pathogens, which kill patients. Viral co-infections (including Epstein-Barr virus, Human Herpes Virus 6, etc.) are found in all the diseases the Marshall Protocol treats, but the viruses are not believed to bethe proximate cause of disease.
+===== CD38 =====
-===== AIDS patients on the Marshall Protocol =====
+CD38 plays a role in effective containment of mycobacteria within granulomata and polarization of Th1 immune responses against Mycobacterium avium. (({{pubmed>long:17533152}}))
+...
+Absence of CD38 rendered mice more susceptible to mycobacterial infection. This susceptibility seems to be due to ineffective Th1 differentiation and polarization, which is essential for the control of M. avium infection. In addition, absence of CD38 seems to compromise the maintenance of the granulomatous barrier, leading to dissemination and unrestrained growth of mycobacteria.
+...
+CD38 Controls the Innate Immune Response against [[https://iai.asm.org/content/81/11/4091|Listeria monocytogenes]]
+Using a murine Listeria monocytogenes infection model, we found that CD38 knockout (KO) mice were highly susceptible to infection. Enhanced susceptibility was already evident within 3 days of infection, suggesting a function of CD38 in the innate immune response.
+CD38 was expressed on neutrophils and inflammatory monocytes, and especially inflammatory monocytes further upregulated CD38 during infection. Absence of CD38 caused alterations of the migration pattern of both cell types to sites of infection.
+...
+In vitro, macrophages of CD38 KO mice were less efficient in uptake of listeria but still able to kill the bacteria. Dendritic cells also displayed enhanced CD38 expression following infection. However, absence of CD38 did not impair the capacity of mice to prime CD8+ T cells against L. monocytogenes, and CD38 KO mice could efficiently control secondary listeria infection. In conclusion, our results demonstrate an essential role for CD38 in the innate immune response against L. monocytogenes.
+===== At this time there are no AIDS patients on the Marshall Protocol =====
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 [[https://journals.lww.com/aidsonline/Fulltext/2000/06160/Role_of_CD38_in_HIV_1_infection__an_epiphenomenon.4.aspx|Signals delivered by CD38]]
-The role of CD38 as a signaling molecule is suggested by the observation that CD38 triggering is involved in T cell costimulation, B cell maturation, and induction of cytokine production by several cell types   (Table 1). These signals are not a prerogative of a single cell lineage but are shared by B, T, and myeloid cells. CD38 signaling inhibits the growth of immature B cells in the bone marrow microenvironment, suggesting that it represents a novel regulatory mechanism of B lymphopoiesis . In mature germinal center B cells, CD38 delivers rescue signals that protect cells from apoptosis and upregulate Bcl-2 (a molecule associated with antiapoptotic effects) in a manner similar to that observed with triggering of CD40, which is known to deliver costimulatory signals to the B cell . In purified T cells, CD38 signaling induces production of high levels of interleukin (IL) 6, granulocyte-macrophage colony-stimulating factor, interferon γ, and IL-10 and low levels of IL-4 and IL-2 (i.e., a cytokine profile shared by T helper 1 and 2 cells) .
+The role of CD38 as a signaling molecule is suggested by the observation that CD38 triggering is involved in T cell costimulation, B cell maturation, and induction of cytokine production by several cell types   (Table 1). These signals are not a prerogative of a single cell lineage but are shared by B, T, and myeloid cells. CD38 signaling inhibits the growth of immature B cells in the bone marrow microenvironment, suggesting that it represents a novel regulatory mechanism of B lymphopoiesis .
-...
-CD38 expression in HIV-1-infected individuals
+In mature germinal center B cells, CD38 delivers rescue signals that protect cells from apoptosis and upregulate Bcl-2 (a molecule associated with antiapoptotic effects) in a manner similar to that observed with triggering of CD40, which is known to deliver costimulatory signals to the B cell . In purified T cells, CD38 signaling induces production of high levels of interleukin (IL) 6, granulocyte-macrophage colony-stimulating factor, interferon γ, and IL-10 and low levels of IL-4 and IL-2 (i.e., a cytokine profile shared by T helper 1 and 2 cells) .
+CD38 expression in HIV-1-infected individuals:
 As in most viral infections, HIV-1 infection causes activation of B and T cells (both CD4 and CD8 cells), which consequently upregulates the surface expression of CD38 and other activation markers. CD38 upregulation can be detected on uninfected cells, indicating that this expression is not caused by direct infection.

home/diseases/hiv_and_aids.txt · Last modified: 09.14.2022 by 127.0.0.1