Isolation of CD45RO+, Memory T Cells Recognizing Proteolipid Protein from Neurologically Normal Subjects

Burns, James; Bartholomew, Breck; Lobo, Stephen

doi:10.1006/cimm.2001.1842

Cited by 8 publications

(7 citation statements)

References 42 publications

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“…Thus, would encephalitogenic T cells build up memory against autoantigens, and if so, do memory cells play a role in the course of chronic or relapsing autoimmune disease? The long-lasting persistence of autoimmune T cell clones in human blood (22)(23)(24), and the memory phenotype displayed by at least some of these cells (25)(26)(27) may argue in favor of autoimmune memory. The opposite prediction would come from EAE studies, where priming of rats with MBP in CFA or IFA confers protection from subsequent EAE induction, but does not prime for enhanced inducibility (28).…”

Section: Discussionmentioning

confidence: 99%

Autoimmune CD4+ T Cell Memory: Lifelong Persistence of Encephalitogenic T Cell Clones in Healthy Immune Repertoires

Kawakami

Odoardi

Ziemssen

et al. 2005

The Journal of Immunology

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We embedded green fluorescent CD4+ T cells specific for myelin basic protein (MBP) (TMBP-GFP cells) in the immune system of syngeneic neonatal rats. These cells persisted in the animals for the entire observation period spanning >2 years without affecting the health of the hosts. They maintained a memory phenotype with low levels of L-selectin and CD45RC, but high CD44. Although persisting in low numbers (0.01–0.1% of lymph node cells) they were sufficient to raise susceptibility toward clinical autoimmune disease. Immunization with MBP in IFA induced CNS inflammation and overt clinical disease in animals carrying neonatally transferred TMBP-GFP cells, but not in controls. The onset of the clinical disease coincided with mass infiltration of TMBP-GFP cells into the CNS. In the periphery, following the amplification phase a rapid contraction of the T cell population was observed. However, elevated numbers of fully reactive TMBP-GFP cells remained in the peripheral immune system after acute experimental autoimmune encephalomyelitis mediating reimmunization-induced disease relapses.

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Section: Discussionmentioning

confidence: 99%

Autoimmune CD4+ T Cell Memory: Lifelong Persistence of Encephalitogenic T Cell Clones in Healthy Immune Repertoires

Kawakami

Odoardi

Ziemssen

et al. 2005

The Journal of Immunology

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“…Clearly the presence of these cells in healthy normal subjects is not sufficient to cause MS. It has been shown that a substantial proportion of PLP-reactive cells in healthy individuals are CD45RO + memory T cells, suggesting that they can be activated in vivo without resulting in clinical disease [49]. In patients with MS, there was less difference in the proportion of female and males subjects with increased T-cell reactivity to PLP peptides than in controls.…”

Section: Discussionmentioning

confidence: 99%

Effect of gender on T-cell proliferative responses to myelin proteolipid protein antigens in patients with multiple sclerosis and controls

Greer

Csurhes

Pender

et al. 2004

Journal of Autoimmunity

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Multiple sclerosis (MS) is an inflammatory demyelinating disorder of the central nervous system. Gender influences both susceptibility to MS, with the disease being more common in women, and the clinical course of disease, with an increased proportion of males developing the primary progressive form of the disease. The basis for these differences may include genetic and immunological factors, and the immunological differences between men and women may be influenced by the effects of the sex hormones. Over several years we have collected blood from MS patients and controls, and measured T-cell responses to myelin proteolipid protein (PLP) and myelin basic protein (MBP) and have shown increased responses to PLP in MS patients compared to healthy controls and patients with other neurological diseases. In the present study we analyzed data from over 500 individuals, to determine whether there are differences between males and females in their responses to PLP and MBP. We found that there was higher frequency of increased T-cell reactivity to immunodominant PLP peptides in women than in men, particularly in non-MS individuals. We suggest that this may be relevant to the higher prevalence of MS in women.

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“…Myelin-reactive T cells from the blood of MS patients show stem/memory-like properties, with reduced need for co-stimulation, suggesting signs of previous activation [9][10][11][12] . Consistent with these findings, autoreactive and bystander memory-phenotype CD4 + T cells preferentially transfer demyelinating disease in mouse models [13][14][15] .…”

Section: Million Individuals Worldwide Suffer From Multiple Sclerosis...mentioning

confidence: 99%

“…Memory-like CD4 + T cells have been implicated as major orchestrators of autoimmune demyelination in mice and humans [9][10][11][12]14,15,48 . To see if this memory-like profile of OCA-B expressing CD4 + T cells is specific to CNS infiltrating cells, we performed flow cytometry using draining lymph node and splenic T cells from MOG-primed OCA-B-mCherry reporter mice.…”

Section: Oca-b Expressing Cd4 + T Cells Display Pathogenic Stem-like ...mentioning

confidence: 99%

OCA-B promotes autoimmune demyelination through control of stem-like CD4⁺T cells

Hughes,

Syage,

Mehrabad

et al. 2023

Preprint

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SummaryStem-like T cell populations can selectively promote autoimmunity, but the activities that sustain these populations are incompletely understood. Here, we show that T cell-intrinsic loss of the transcription cofactor OCA-B protects mice from experimental autoimmune encephalomyelitis (EAE) while preserving responses to infection. In EAE models driven by antigen re-encounter, OCA-B deletion eliminates CNS infiltration, proinflammatory cytokine production and clinical disease. OCA-B-expressing CD4+T cells within the CNS of mice with EAE display a memory phenotype and preferentially confer disease. In a relapsing-remitting EAE model, OCA-B T cell-deficiency specifically protects mice from relapse. During remission, OCA-B promotes the expression ofTcf7,Slamf6, andSellin proliferating T cell populations. At relapse, OCA-B loss results in both the accumulation of an immunomodulatory CD4+T cell population expressingCcr9andBach2, and the loss of effector gene expression from Th17 cells. These results identify OCA-B as a driver of pathogenic stem-like T cells.

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Isolation of CD45RO+, Memory T Cells Recognizing Proteolipid Protein from Neurologically Normal Subjects

Cited by 8 publications

References 42 publications

Autoimmune CD4+ T Cell Memory: Lifelong Persistence of Encephalitogenic T Cell Clones in Healthy Immune Repertoires

Autoimmune CD4+ T Cell Memory: Lifelong Persistence of Encephalitogenic T Cell Clones in Healthy Immune Repertoires

Effect of gender on T-cell proliferative responses to myelin proteolipid protein antigens in patients with multiple sclerosis and controls

OCA-B promotes autoimmune demyelination through control of stem-like CD4⁺T cells

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Isolation of CD45RO+, Memory T Cells Recognizing Proteolipid Protein from Neurologically Normal Subjects

Cited by 8 publications

References 42 publications

Autoimmune CD4+ T Cell Memory: Lifelong Persistence of Encephalitogenic T Cell Clones in Healthy Immune Repertoires

Autoimmune CD4+ T Cell Memory: Lifelong Persistence of Encephalitogenic T Cell Clones in Healthy Immune Repertoires

Effect of gender on T-cell proliferative responses to myelin proteolipid protein antigens in patients with multiple sclerosis and controls

OCA-B promotes autoimmune demyelination through control of stem-like CD4+T cells

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OCA-B promotes autoimmune demyelination through control of stem-like CD4⁺T cells