Stimulation or tolerization of an anti-myelin basic protein T lymphocyte line with membrane fragments from antigen presenting cells

Jm, Boggs; Nh, Chang; Goundalkar, Ashok; Ga, Hashim

doi:10.1016/0008-8749(92)90003-8

Cited by 8 publications

(3 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One of the best characterized co-stimulatory molecules expressed by T cells is CD28, which interacts with CD80 (B7-1) and CD86 (B7-2) . Studies have demonstrated that the inhibition of CD28-mediated co-stimulation most efficiently induces unresponsiveness of cognate T-lymphocytes [88, 89]. Many groups studied the expression levels of CD80 and CD86 on the surface of ESC and ESC-derived cells, but there is no consensus regarding the expression level.…”

Section: Immunogenicity Of Undifferentiated and Differentiated Stem Cmentioning

confidence: 99%

Immunological Barriers to Stem-Cell Based Cardiac Repair

Karabekian

Posnack

Sarvazyan

2010

Stem Cell Rev and Rep

View full text Add to dashboard Cite

Repair of damaged myocardium with pluripotent stem cell derived cardiomyocytes is becoming increasingly more feasible. Developments in stem cell research emphasize the need to address the foreseeable problem of immune rejection following transplantation. Pluripotent stem cell (PSC) derived cardiomyocytes have unique immune characteristics, some of which are not advantageous for transplantation. Here we review the possible mechanisms of PSC-derived cardiomyocytes rejection, summarize the current knowledge pertaining to immunogenicity of such cells and describe the existing controversies. Myocardial graft rejection can be reduced by modifying PSCs prior to their differentiation into cardiomyocytes. Overall, this approach facilitates the development of universal donor stem cells suitable for the regeneration of many different tissue types.

show abstract

Section: Immunogenicity Of Undifferentiated and Differentiated Stem Cmentioning

confidence: 99%

Immunological Barriers to Stem-Cell Based Cardiac Repair

Karabekian

Posnack

Sarvazyan

2010

Stem Cell Rev and Rep

View full text Add to dashboard Cite

show abstract

“…Other experimental therapies have also successfully targeted the TMC in EAE by either including inactivated carrier cells such as spleen cells that had been coupled with antigen [57,58,134,135] or by soluble MHC-peptide complexes [126] or by the administration of membrane fragments of cells that have been prepulsed with protein l0 R. Martin, H. McFmland [13]. These methods have led to an anergic state since encephalitogenic T cells are not properly activated in the absence of co-stimulatory signals.…”

Section: Treatments Inducing Functional Changes In Encephalitogenie Tmentioning

confidence: 99%

Experimental immunotherapies for multiple sclerosis

Martin

McFarland

1996

Springer Semin Immunopathol

View full text Add to dashboard Cite

Multiple sclerosis (MS) is a chronic demyelinating disease affecting the central nervous system (CNS) principally in young adults. Although its etiology is as yet unknown current evidence suggests that tissue damage is mediated by autoimmune T cells. The examination of an experimental animal model for MS, experimental allergic encephalomyelitis (EAE), has demonstrated that myelin basic protein (MBP)- or proteolipid protein (PLP)-specific T cells mediate the destruction of CNS myelin. In recent years, elegant studies in EAE have shown that encephalitogenic T cells recognize short peptides of MBP or PLP in the context of MHC/HLA-class II molecules, express a restricted number of T cell receptor (TCR) molecules and secrete interferon-gamma and tumor necrosis factor-alpha/beta. Understanding the pathogenetic steps in lesion development at the molecular level led to highly specific immunotherapies for EAE targeting each individual molecule. It has been the hope of many investigators that immunological events resembling those in EAE can be found in patients with MS and that the specific immunotherapies effective in EAE could also be applied to MS. However, to date, the evidence for a unique immunological abnormality in MS is not strong. Although MBP- and PLP-specific T cells with properties similar to those that are encephalitogenic in animals can be isolated from patients, they are not specific for MS and occur with similar frequency in controls. In addition, the variability in specificity and TCR usage has raised questions regarding the relevance of these cells in patients. The importance of the T cell responses to myelin antigens in MS may not be established until the effects of abrogating their activity through specific therapies targeting the trimolecular complex (TMC) have been demonstrated. Consequently, attention has begun to focus on modifying the biology of the MS lesion rather than targeting the initiating event at the level of the TMC, and the success of this approach is reflected by the effect of interferon-beta on lesion development in MS. The recent approval for the use of interferon-beta for the treatment of relapsing-remitting MS has raised great interest in examining novel strategies for immunotherapies in MS. The basic concepts as well as the current candidates for such new immunotherapies will be outlined in this short review.

show abstract

“…Mouse body weight = 20 g, monkey = 3 kg, human assumed to be 70 kg 2. Conversion factors: mouse, µg/m 2 = µg/kg × 3; monkey, µg/m 2 = µg/kg × 12; human, µg/m 2 = µg/kg × 40.…”

mentioning

confidence: 99%