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Anna Erlandsson - One of the best experts on this subject based on the ideXlab platform.

  • Astrocytes have the Capacity to Act as antigen-presenting cells in the Parkinson’s disease brain
    Journal of neuroinflammation, 2020
    Co-Authors: Jinar Rostami, Grammatiki Fotaki, Julien Sirois, Ropafadzo Mzezewa, Joakim Bergström, Magnus Essand, Luke M. Healy, Anna Erlandsson
    Abstract:

    Many lines of evidence suggest that accumulation of aggregated alpha-synuclein (αSYN) in the Parkinson’s disease (PD) brain causes infiltration of T cells. However, in which ways the stationary brain cells interAct with the T cells remain elusive. Here, we identify astrocytes as potential antigen-presenting cells capable of Activating T cells in the PD brain. Astrocytes are a major component of the nervous system, and accumulating data indicate that astrocytes can play a central role during PD progression. to investigate the role of astrocytes in antigen presentation and T-cell Activation in the PD brain, we analyzed post mortem brain tissue from PD patients and controls. Moreover, we studied the Capacity of cultured human astrocytes and adult human microglia to Act as professional antigen-presenting cells following exposure to preformed αSYN fibrils. Our analysis of post mortem brain tissue demonstrated that PD patients express high levels of MHC-II, which correlated with the load of pathological, phosphorylated αSYN. Interestingly, a very high proportion of the MHC-II co-localized with astrocytic markers. Importantly, we found both perivascular and infiltrated CD4+ T cells to be surrounded by MHC-II expressing astrocytes, confirming an astrocyte T cell cross-talk in the PD brain. Moreover, we showed that αSYN accumulation in cultured human astrocytes triggered surface expression of co-stimulatory molecules critical for T-cell Activation, while cultured human microglia displayed very poor antigen presentation Capacity. Notably, intercellular transfer of αSYN/MHC-II deposits occurred between astrocytes via tunneling nanotubes, indicating spreading of inflammation in addition to toxic protein aggregates. In conclusion, our data from histology and cell culture studies suggest an important role for astrocytes in antigen presentation and T-cell Activation in the PD brain, highlighting astrocytes as a promising therapeutic target in the context of chronic inflammation.

  • astrocytes have the Capacity to Act as antigen presenting cells in the parkinson s disease brain
    Journal of Neuroinflammation, 2020
    Co-Authors: Jinar Rostami, Grammatiki Fotaki, Julien Sirois, Ropafadzo Mzezewa, Joakim Bergström, Magnus Essand, Luke M. Healy, Anna Erlandsson
    Abstract:

    Many lines of evidence suggest that accumulation of aggregated alpha-synuclein (αSYN) in the Parkinson’s disease (PD) brain causes infiltration of T cells. However, in which ways the stationary brain cells interAct with the T cells remain elusive. Here, we identify astrocytes as potential antigen-presenting cells capable of Activating T cells in the PD brain. Astrocytes are a major component of the nervous system, and accumulating data indicate that astrocytes can play a central role during PD progression. to investigate the role of astrocytes in antigen presentation and T-cell Activation in the PD brain, we analyzed post mortem brain tissue from PD patients and controls. Moreover, we studied the Capacity of cultured human astrocytes and adult human microglia to Act as professional antigen-presenting cells following exposure to preformed αSYN fibrils. Our analysis of post mortem brain tissue demonstrated that PD patients express high levels of MHC-II, which correlated with the load of pathological, phosphorylated αSYN. Interestingly, a very high proportion of the MHC-II co-localized with astrocytic markers. Importantly, we found both perivascular and infiltrated CD4+ T cells to be surrounded by MHC-II expressing astrocytes, confirming an astrocyte T cell cross-talk in the PD brain. Moreover, we showed that αSYN accumulation in cultured human astrocytes triggered surface expression of co-stimulatory molecules critical for T-cell Activation, while cultured human microglia displayed very poor antigen presentation Capacity. Notably, intercellular transfer of αSYN/MHC-II deposits occurred between astrocytes via tunneling nanotubes, indicating spreading of inflammation in addition to toxic protein aggregates. In conclusion, our data from histology and cell culture studies suggest an important role for astrocytes in antigen presentation and T-cell Activation in the PD brain, highlighting astrocytes as a promising therapeutic target in the context of chronic inflammation.

Jinar Rostami - One of the best experts on this subject based on the ideXlab platform.

  • Astrocytes have the Capacity to Act as antigen-presenting cells in the Parkinson’s disease brain
    Journal of neuroinflammation, 2020
    Co-Authors: Jinar Rostami, Grammatiki Fotaki, Julien Sirois, Ropafadzo Mzezewa, Joakim Bergström, Magnus Essand, Luke M. Healy, Anna Erlandsson
    Abstract:

    Many lines of evidence suggest that accumulation of aggregated alpha-synuclein (αSYN) in the Parkinson’s disease (PD) brain causes infiltration of T cells. However, in which ways the stationary brain cells interAct with the T cells remain elusive. Here, we identify astrocytes as potential antigen-presenting cells capable of Activating T cells in the PD brain. Astrocytes are a major component of the nervous system, and accumulating data indicate that astrocytes can play a central role during PD progression. to investigate the role of astrocytes in antigen presentation and T-cell Activation in the PD brain, we analyzed post mortem brain tissue from PD patients and controls. Moreover, we studied the Capacity of cultured human astrocytes and adult human microglia to Act as professional antigen-presenting cells following exposure to preformed αSYN fibrils. Our analysis of post mortem brain tissue demonstrated that PD patients express high levels of MHC-II, which correlated with the load of pathological, phosphorylated αSYN. Interestingly, a very high proportion of the MHC-II co-localized with astrocytic markers. Importantly, we found both perivascular and infiltrated CD4+ T cells to be surrounded by MHC-II expressing astrocytes, confirming an astrocyte T cell cross-talk in the PD brain. Moreover, we showed that αSYN accumulation in cultured human astrocytes triggered surface expression of co-stimulatory molecules critical for T-cell Activation, while cultured human microglia displayed very poor antigen presentation Capacity. Notably, intercellular transfer of αSYN/MHC-II deposits occurred between astrocytes via tunneling nanotubes, indicating spreading of inflammation in addition to toxic protein aggregates. In conclusion, our data from histology and cell culture studies suggest an important role for astrocytes in antigen presentation and T-cell Activation in the PD brain, highlighting astrocytes as a promising therapeutic target in the context of chronic inflammation.

  • astrocytes have the Capacity to Act as antigen presenting cells in the parkinson s disease brain
    Journal of Neuroinflammation, 2020
    Co-Authors: Jinar Rostami, Grammatiki Fotaki, Julien Sirois, Ropafadzo Mzezewa, Joakim Bergström, Magnus Essand, Luke M. Healy, Anna Erlandsson
    Abstract:

    Many lines of evidence suggest that accumulation of aggregated alpha-synuclein (αSYN) in the Parkinson’s disease (PD) brain causes infiltration of T cells. However, in which ways the stationary brain cells interAct with the T cells remain elusive. Here, we identify astrocytes as potential antigen-presenting cells capable of Activating T cells in the PD brain. Astrocytes are a major component of the nervous system, and accumulating data indicate that astrocytes can play a central role during PD progression. to investigate the role of astrocytes in antigen presentation and T-cell Activation in the PD brain, we analyzed post mortem brain tissue from PD patients and controls. Moreover, we studied the Capacity of cultured human astrocytes and adult human microglia to Act as professional antigen-presenting cells following exposure to preformed αSYN fibrils. Our analysis of post mortem brain tissue demonstrated that PD patients express high levels of MHC-II, which correlated with the load of pathological, phosphorylated αSYN. Interestingly, a very high proportion of the MHC-II co-localized with astrocytic markers. Importantly, we found both perivascular and infiltrated CD4+ T cells to be surrounded by MHC-II expressing astrocytes, confirming an astrocyte T cell cross-talk in the PD brain. Moreover, we showed that αSYN accumulation in cultured human astrocytes triggered surface expression of co-stimulatory molecules critical for T-cell Activation, while cultured human microglia displayed very poor antigen presentation Capacity. Notably, intercellular transfer of αSYN/MHC-II deposits occurred between astrocytes via tunneling nanotubes, indicating spreading of inflammation in addition to toxic protein aggregates. In conclusion, our data from histology and cell culture studies suggest an important role for astrocytes in antigen presentation and T-cell Activation in the PD brain, highlighting astrocytes as a promising therapeutic target in the context of chronic inflammation.

Hans J. Van Der Vliet - One of the best experts on this subject based on the ideXlab platform.

Niels C. Bols - One of the best experts on this subject based on the ideXlab platform.

  • development of a zebrafish spleen cell line zssj and its growth arrest by gamma irradiation and Capacity to Act as feeder cells
    In Vitro Cellular & Developmental Biology – Animal, 2009
    Co-Authors: J. G. Xing, C. Seymour, W Elsweisi, Paul Collodi, Carmel Mothersill, Niels C. Bols
    Abstract:

    A zebrafish spleen cell line, ZSSJ, was developed and its growth arrest by gamma radiation determined and its Capacity to stimulate the proliferation of the zebrafish blastula cell line, ZEB2J, measured. ZSSJ was initiated by explant outgrowth, grew adherent with mainly an epithelial-like morphology, and stained strongly for alkaline phosphatase. ZSSJ was not only grown in L-15 with 15% fetal bovine serum at 26°C to 28°°C but also grew at room temperature. Cultures of ZSSJ have undergone approximately 40 population doublings, had few cells staining for b-galactosidase Activity, which is commonly present in senescent cultures, and many cells with an aneuploid karyotype, which is frequently associated with immortalization. ZSSJ growth was arrested by 30 to 50 Gy of g-irradiation, whereas after 20 Gy, some slight growth was observed. By contrast, growth of the rainbow trout spleen stromal cell line, RTS34st, which has been used as a feeder for zebrafish ES cell cultures, was arrested completely by 20 Gy. In cocultures, nongrowth-arrested ZSSJ stimulated ZEB2J proliferation better than growth-arrested ZSSJ and better than RTS34st. ZSSJ should be useful as a feeder cell line for zebrafish ES cell cultures.

  • Development of a zebrafish spleen cell line, ZSSJ, and its growth arrest by gamma irradiation and Capacity to Act as feeder cells
    In Vitro Cellular and Developmental Biology - Animal, 2009
    Co-Authors: J. G. Xing, W. El-sweisi, L. E.j. Lee, C. Seymour, Paul Collodi, Carmel Mothersill, Niels C. Bols
    Abstract:

    A zebrafish spleen cell line, ZSSJ, was developed and its growth arrest by gamma radiation determined and its Capacity to stimulate the proliferation of the zebrafish blastula cell line, ZEB2J, measured. ZSSJ was initiated by explant outgrowth, grew adherent with mainly an epithelial-like morphology, and stained strongly for alkaline phosphatase. ZSSJ was not only grown in L-15 with 15% fetal bovine serum at 26 degrees C to 28 degrees degrees C but also grew at room temperature. Cultures of ZSSJ have undergone approximately 40 population doublings, had few cells staining for b-galactosidase Activity, which is commonly present in senescent cultures, and many cells with an aneuploid karyotype, which is frequently associated with immortalization. ZSSJ growth was arrested by 30 to 50 Gy of g-irradiation, whereas after 20 Gy, some slight growth was observed. By contrast, growth of the rainbow trout spleen stromal cell line, RTS34st, which has been used as a feeder for zebrafish ES cell cultures, was arrested completely by 20 Gy. In cocultures, nongrowth-arrested ZSSJ stimulated ZEB2J proliferation better than growth-arrested ZSSJ and better than RTS34st. ZSSJ should be useful as a feeder cell line for zebrafish ES cell cultures.

Grammatiki Fotaki - One of the best experts on this subject based on the ideXlab platform.

  • Astrocytes have the Capacity to Act as antigen-presenting cells in the Parkinson’s disease brain
    Journal of neuroinflammation, 2020
    Co-Authors: Jinar Rostami, Grammatiki Fotaki, Julien Sirois, Ropafadzo Mzezewa, Joakim Bergström, Magnus Essand, Luke M. Healy, Anna Erlandsson
    Abstract:

    Many lines of evidence suggest that accumulation of aggregated alpha-synuclein (αSYN) in the Parkinson’s disease (PD) brain causes infiltration of T cells. However, in which ways the stationary brain cells interAct with the T cells remain elusive. Here, we identify astrocytes as potential antigen-presenting cells capable of Activating T cells in the PD brain. Astrocytes are a major component of the nervous system, and accumulating data indicate that astrocytes can play a central role during PD progression. to investigate the role of astrocytes in antigen presentation and T-cell Activation in the PD brain, we analyzed post mortem brain tissue from PD patients and controls. Moreover, we studied the Capacity of cultured human astrocytes and adult human microglia to Act as professional antigen-presenting cells following exposure to preformed αSYN fibrils. Our analysis of post mortem brain tissue demonstrated that PD patients express high levels of MHC-II, which correlated with the load of pathological, phosphorylated αSYN. Interestingly, a very high proportion of the MHC-II co-localized with astrocytic markers. Importantly, we found both perivascular and infiltrated CD4+ T cells to be surrounded by MHC-II expressing astrocytes, confirming an astrocyte T cell cross-talk in the PD brain. Moreover, we showed that αSYN accumulation in cultured human astrocytes triggered surface expression of co-stimulatory molecules critical for T-cell Activation, while cultured human microglia displayed very poor antigen presentation Capacity. Notably, intercellular transfer of αSYN/MHC-II deposits occurred between astrocytes via tunneling nanotubes, indicating spreading of inflammation in addition to toxic protein aggregates. In conclusion, our data from histology and cell culture studies suggest an important role for astrocytes in antigen presentation and T-cell Activation in the PD brain, highlighting astrocytes as a promising therapeutic target in the context of chronic inflammation.

  • astrocytes have the Capacity to Act as antigen presenting cells in the parkinson s disease brain
    Journal of Neuroinflammation, 2020
    Co-Authors: Jinar Rostami, Grammatiki Fotaki, Julien Sirois, Ropafadzo Mzezewa, Joakim Bergström, Magnus Essand, Luke M. Healy, Anna Erlandsson
    Abstract:

    Many lines of evidence suggest that accumulation of aggregated alpha-synuclein (αSYN) in the Parkinson’s disease (PD) brain causes infiltration of T cells. However, in which ways the stationary brain cells interAct with the T cells remain elusive. Here, we identify astrocytes as potential antigen-presenting cells capable of Activating T cells in the PD brain. Astrocytes are a major component of the nervous system, and accumulating data indicate that astrocytes can play a central role during PD progression. to investigate the role of astrocytes in antigen presentation and T-cell Activation in the PD brain, we analyzed post mortem brain tissue from PD patients and controls. Moreover, we studied the Capacity of cultured human astrocytes and adult human microglia to Act as professional antigen-presenting cells following exposure to preformed αSYN fibrils. Our analysis of post mortem brain tissue demonstrated that PD patients express high levels of MHC-II, which correlated with the load of pathological, phosphorylated αSYN. Interestingly, a very high proportion of the MHC-II co-localized with astrocytic markers. Importantly, we found both perivascular and infiltrated CD4+ T cells to be surrounded by MHC-II expressing astrocytes, confirming an astrocyte T cell cross-talk in the PD brain. Moreover, we showed that αSYN accumulation in cultured human astrocytes triggered surface expression of co-stimulatory molecules critical for T-cell Activation, while cultured human microglia displayed very poor antigen presentation Capacity. Notably, intercellular transfer of αSYN/MHC-II deposits occurred between astrocytes via tunneling nanotubes, indicating spreading of inflammation in addition to toxic protein aggregates. In conclusion, our data from histology and cell culture studies suggest an important role for astrocytes in antigen presentation and T-cell Activation in the PD brain, highlighting astrocytes as a promising therapeutic target in the context of chronic inflammation.