Possible Causes Of Autoimmune Disease

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Tanaka and colleagues now hope to better understand this proteins function by clarifying the regulatory factors that act upstream and downstream of PDLIM2 and by clarifying how this system influences other inflammatory processes such as those observed in cases of asthma or during wound healing. More information: Tanaka T. et al.

More recently other researchers identified a population of helper T cells called TH17 cells that also contribute to this process although their role was unclear so Tanaka sought to determine whether PDLIM2 regulates these cells as well. Possible Causes Of Autoimmune Disease his team found that mice lacking the gene encoding PDLIM2 formed many more granulomas in response to infection with Propionibacterium acnes bacteria Fig. 1 and that this process was dependent on the action of TH17 cells. In fact the researchers showed that PDLIM2 directly inhibits the differentiation of CD4+ T cells into TH17 cells as was previously demonstrated with TH1 development. This protein works by marking other proteins for rapid degradation. Tanaka and colleagues learned that PDLIM2 specifically promotes the destruction of STAT3 a signaling protein that switches on genes responsible for TH17 development. Without PDLIM2 constraining the formation of these pro-inflammatory cells the immune response has the potential to spiral out of control.

In collaboration with Tadashi Matsuda of Hokkaido University Tanakas group has now revealed a key regulatory checkpoint in the granuloma formation process which might ultimately inform the development of more effective immunomodulatory drugs. Historically a subset of the immune systems helper T cells called TH1 cells has been associated with autoimmunity. Previous research by Tanaka demonstrated that a protein called PDLIM helps restrict production of these cells2 –

  • This protein therefore appears to be a key safeguard against autoimmunity
  • Without PDLIM2 constraining the formation of these pro-inflammatory cells the immune response has the potential to spiral out of control
  • In collaboration with Tadashi Matsuda of Hokkaido University Tanakas group has now revealed a key regulatory checkpoint in the granuloma formation process which might ultimately inform the development of more effective immunomodulatory drugs
  • TH17 cells
  • More information: Tanaka T
  • His team found that mice lacking the gene encoding PDLIM2 formed many more granulomas in response to infection with Propionibacterium acnes bacteria Fig

. More recently other researchers identified a population of helper T cells called TH17 cells that also contribute to this process although their role was unclear so Tanaka sought to determine whether PDLIM2 regulates these cells as well.

More recently other researchers identified a population of helper T cells called TH17 cells that also contribute to this process although their role was unclear so Tanaka sought to determine whether PDLIM2 regulates these cells

Possible Causes Of Autoimmune Disease

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as well. His team found that mice lacking the gene encoding PDLIM2 formed many more granulomas in response to infection with Propionibacterium acnes bacteria Fig. 1 and that this Possible Causes Of Autoimmune Disease process was dependent on the action of TH17 cells. In fact the researchers showed that PDLIM2 directly inhibits the differentiation of CD4+ T cells into TH17 cells as was previously demonstrated with TH1 development. This protein works by marking other proteins for rapid degradation. Tanaka and colleagues learned that PDLIM2 specifically promotes the destruction of STAT3 a signaling protein that switches on genes responsible for TH17 development. Without PDLIM2 constraining the formation of these pro-inflammatory cells the immune response has the potential to spiral out of control.

Tanaka and colleagues learned that PDLIM2 specifically promotes the destruction of STAT3 a signaling protein that switches on genes responsible for TH17 development. Without Possible Causes Of Autoimmune Disease PDLIM2 constraining the formation of these pro-inflammatory cells the immune response has the potential to spiral out of control. This protein therefore appears to be a key safeguard against autoimmunity.

Tanaka and colleagues now hope to better understand this proteins function by clarifying the regulatory factors that act upstream and downstream of PDLIM2 and by clarifying how this system influences other inflammatory processes such as those observed in cases of asthma or during wound healing. More information: Tanaka T. et al.

Previous research by Tanaka demonstrated that a protein called PDLIM helps restrict production of these cells2. More recently other researchers identified a population of helper T cells called TH17 cells that also contribute to this process although their role was unclear so Tanaka sought to determine whether PDLIM2 regulates these cells as well. His team found that micelacking the gene encoding PDLIM2 formed many more granulomas in response to infection with Propionibacterium acnes bacteria Fig. 1 and that this process was dependent on the action of TH17 cells. In fact the researchers showed that PDLIM2 directly inhibits the differentiation Possible Causes Of Autoimmune Disease of CD4+ T cells into TH17 cells as was previously demonstrated with TH1 development. This protein works by marking other proteins for rapid degradation.

Tanaka and colleagues now hope to better understand this proteins function by clarifying the regulatory factors that act upstream and downstream of PDLIM2 and by clarifying how this system influences other inflammatory processes such as those observed in cases of asthma or during wound healing. More information: Tanaka T. et al.

Previous research by Tanaka demonstrated that a protein called PDLIM helps restrict production of these cells2. More recently other researchers identified a population of helper T cells called TH17 cells that also contribute to this process although their role was unclear so Tanaka sought to determine whether PDLIM2 regulates these cells as well. His team found that mice lacking the gene encoding PDLIM2 formed many more granulomas in response to infection with Propionibacterium acnes bacteria Fig.

A central regulator of the inflammatory response shows signs as a target for therapies against autoimmune disease Granulomas are indicated by dark spots formed following staining with hematoxylin and eosin scale bars 100 m. Credit: Reproduced from Ref. 1 2012 AAASSome bacterial infections trigger the formation of structures known as granulomas which essentially quarantine compromised cells. This response is generally beneficial but can lead to a harmful overreaction especially in patients with autoimmune conditions where the inflammatory response is not properly regulated.

This

response is generally beneficial but can lead to a harmful overreaction especially in patients with autoimmune conditions where the inflammatory response is not properly regulated. In collaboration with Tadashi Matsuda of Hokkaido University Tanakas group has now revealed a key regulatory checkpoint in the granuloma formation process which might ultimately inform the development of more effective immunomodulatory drugs. Historically a subset of the immune systems helper T cells called TH1 cells has been associated with autoimmunity.

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