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  1. Article ; Online: Indoctrinating T cells to attack pathogens through homeschooling.

    Parello, Caitlin S / Huseby, Eric S

    Trends in immunology

    2015  Volume 36, Issue 6, Page(s) 337–343

    Abstract: Adaptive immunity is predicated on the ability of the T cell repertoire to have pre-existing specificity for the universe of potential pathogens. Recent findings suggest that T cell receptor (TCR)-self-major histocompatibility protein (pMHC) interactions ...

    Abstract Adaptive immunity is predicated on the ability of the T cell repertoire to have pre-existing specificity for the universe of potential pathogens. Recent findings suggest that T cell receptor (TCR)-self-major histocompatibility protein (pMHC) interactions limit autoimmune responses while enhancing T cell response to foreign antigens. We review these findings here, placing them in context of the current understanding of how TCR-self-pMHC interactions regulate T cell activation thresholds, and suggest that TCR-self-pMHC interactions increase the efficiency of the T cell repertoire by giving a competitive advantage to peptide cross-reactive T cells. We propose that self-reactivity and peptide cross-reactivity are controlled by particular CDR3 sequence motifs, which would allow thymic selection to contribute to solving the feat of broad pathogen specificity by exporting T cells that are pre-screened by positive and negative selection for the ability to be 'moderately' peptide cross-reactive.
    MeSH term(s) Adaptive Immunity/immunology ; Animals ; Antigen-Presenting Cells/immunology ; Autoimmunity/immunology ; Humans ; Major Histocompatibility Complex/immunology ; Models, Immunological ; Peptides/immunology ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/immunology
    Chemical Substances Peptides ; Receptors, Antigen, T-Cell
    Language English
    Publishing date 2015-06
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2036831-8
    ISSN 1471-4981 ; 1471-4906
    ISSN (online) 1471-4981
    ISSN 1471-4906
    DOI 10.1016/j.it.2015.04.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Role of T cell-glial cell interactions in creating and amplifying central nervous system inflammation and multiple sclerosis disease symptoms.

    Huseby, Eric S / Kamimura, Daisuke / Arima, Yasunobu / Parello, Caitlin S / Sasaki, Katsuhiro / Murakami, Masaaki

    Frontiers in cellular neuroscience

    2015  Volume 9, Page(s) 295

    Abstract: Multiple Sclerosis (MS) is an inflammatory disease of the Central Nervous System (CNS) that causes the demyelination of nerve cells and destroys oligodendrocytes, neurons and axons. Historically, MS has been thought of as a T cell-mediated autoimmune ... ...

    Abstract Multiple Sclerosis (MS) is an inflammatory disease of the Central Nervous System (CNS) that causes the demyelination of nerve cells and destroys oligodendrocytes, neurons and axons. Historically, MS has been thought of as a T cell-mediated autoimmune disease of CNS white matter. However, recent studies have identified gray matter lesions in MS patients, suggesting that CNS antigens other than myelin proteins may be involved during the MS disease process. We have recently found that T cells targeting astrocyte-specific antigens can drive unique aspects of inflammatory CNS autoimmunity, including the targeting of gray matter and white matter of the brain and inducing heterogeneous clinical disease courses. In addition to being a target of T cells, astrocytes play a critical role in propagating the inflammatory response within the CNS induced NF-κB signaling. Here, we will discuss the pathophysiology of CNS inflammation mediated by T cell-glial cell interactions and its contributions to CNS autoimmunity.
    Language English
    Publishing date 2015-08-05
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2015.00295
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Shiga toxin 2-induced endoplasmic reticulum stress is minimized by activated protein C but does not correlate with lethal kidney injury.

    Parello, Caitlin S L / Mayer, Chad L / Lee, Benjamin C / Motomochi, Amanda / Kurosawa, Shinichiro / Stearns-Kurosawa, Deborah J

    Toxins

    2015  Volume 7, Issue 1, Page(s) 170–186

    Abstract: Enterohemorrhagic Escherichia coli produce ribotoxic Shiga toxins (Stx), which are responsible for kidney injury and development of hemolytic uremic syndrome. The endoplasmic reticulum (ER) stress response is hypothesized to induce apoptosis contributing ...

    Abstract Enterohemorrhagic Escherichia coli produce ribotoxic Shiga toxins (Stx), which are responsible for kidney injury and development of hemolytic uremic syndrome. The endoplasmic reticulum (ER) stress response is hypothesized to induce apoptosis contributing to organ injury; however, this process has been described only in vitro. ER stress marker transcripts of spliced XBP1 (1.78-fold), HSP40 (4.45-fold) and CHOP (7.69-fold) were up-regulated early in kidneys of Stx2 challenged mice compared to saline controls. Anti-apoptotic Bcl2 decreased (-2.41-fold vs. saline) and pro-apoptotic DR5 increased (6.38-fold vs. saline) at later time points. Cytoprotective activated protein C (APC) reduced early CHOP expression (-3.3-fold vs. untreated), increased later Bcl2 expression (5.8-fold vs. untreated), and had early effects on survival but did not alter DR5 expression. Changes in kidney ER stress and apoptotic marker transcripts were observed in Stx2-producing C. rodentium challenged mice compared to mice infected with a non-toxigenic control strain. CHOP (4.14-fold) and DR5 (2.81-fold) were increased and Bcl2 (-1.65-fold) was decreased. APC reduced CHOP expression and increased Bcl2 expression, but did not alter mortality. These data indicate that Stx2 induces renal ER stress and apoptosis in murine models of Stx2-induced kidney injury, but decreasing these processes alone was not sufficient to alter survival outcome.
    MeSH term(s) Acute Kidney Injury/chemically induced ; Acute Kidney Injury/drug therapy ; Acute Kidney Injury/genetics ; Acute Kidney Injury/pathology ; Animals ; Apoptosis/drug effects ; Citrobacter rodentium ; DNA-Binding Proteins/genetics ; Endoplasmic Reticulum Stress/drug effects ; HSP40 Heat-Shock Proteins/genetics ; Kidney/drug effects ; Kidney/metabolism ; Kidney/pathology ; Mice, Inbred C57BL ; Protein C/pharmacology ; Protein C/therapeutic use ; Proto-Oncogene Proteins c-bcl-2/genetics ; Receptors, TNF-Related Apoptosis-Inducing Ligand/genetics ; Regulatory Factor X Transcription Factors ; Shiga Toxin 2/toxicity ; Transcription Factor CHOP/genetics ; Transcription Factors/genetics ; X-Box Binding Protein 1
    Chemical Substances DNA-Binding Proteins ; Ddit3 protein, mouse ; Dnajb1 protein, mouse ; HSP40 Heat-Shock Proteins ; Protein C ; Proto-Oncogene Proteins c-bcl-2 ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Regulatory Factor X Transcription Factors ; Shiga Toxin 2 ; Transcription Factors ; X-Box Binding Protein 1 ; Xbp1 protein, mouse ; Transcription Factor CHOP (147336-12-7)
    Language English
    Publishing date 2015-01-20
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2518395-3
    ISSN 2072-6651 ; 2072-6651
    ISSN (online) 2072-6651
    ISSN 2072-6651
    DOI 10.3390/toxins7010170
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Pro-Coagulant Endothelial Dysfunction Results from EHEC Shiga Toxins and Host Damage-Associated Molecular Patterns.

    Mayer, Chad L / Parello, Caitlin S L / Lee, Benjamin C / Itagaki, Kiyoshi / Kurosawa, Shinichiro / Stearns-Kurosawa, Deborah J

    Frontiers in immunology

    2015  Volume 6, Page(s) 155

    Abstract: Hemolytic uremic syndrome (HUS) from enterohemorrhagic Escherichia coli infection is a leading cause of kidney failure in otherwise healthy U.S. children. The bacterial Shiga toxins (Stx) induce the characteristic coagulopathy of HUS, but the damage to ... ...

    Abstract Hemolytic uremic syndrome (HUS) from enterohemorrhagic Escherichia coli infection is a leading cause of kidney failure in otherwise healthy U.S. children. The bacterial Shiga toxins (Stx) induce the characteristic coagulopathy of HUS, but the damage to toxin-receptor expressing cells and organ injury due to ischemia likely also releases inflammatory damage-associated molecular patterns (DAMPs), which may exacerbate injury along with the toxins. To examine this, human aortic and renal glomerular cell anti-coagulant and barrier functions were studied after in vitro challenge with Stx1, Stx2, and DAMPs. There was significant loss of surface anti-coagulant protein C pathway molecules, increased expression of pro-thrombotic PAR1 and reduced protein C activation capability by 15-27%. Histones nearly completely prevented the activated protein C protection of endothelial cells from thrombin-induced permeability. In mice, lethal Stx2 challenge elevated plasma HMGB1 (day 2, 321 ± 118%; p < 0.01) and extracellular histones (day 3, 158 ± 62%; p < 0.01). Mice colonized with Stx2-expressing Citrobacter rodentium developed increased HMGB1 (day 5, 155 ± 55%; p < 0.01) and histones (day 3, 378 ± 188%; p < 0.01). Anti-histone antibody reduced both DAMPs to baseline, but was not sufficient to improve survival outcome or kidney function. Together, these data suggest a potential role Stx to produce DAMPs, and DAMPs to produce endothelial injury and a pro-thrombotic environment.
    Language English
    Publishing date 2015
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2606827-8
    ISSN 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2015.00155
    Database MEDical Literature Analysis and Retrieval System OnLINE

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