, a bio/informatics shared resource is still "open for business" - Visit the CDS website


Other search tools

About this data

The publication data currently available has been vetted by Vanderbilt faculty, staff, administrators and trainees. The data itself is retrieved directly from NCBI's PubMed and is automatically updated on a weekly basis to ensure accuracy and completeness.

If you have any questions or comments, please contact us.

Results: 1 to 6 of 6

Publication Record

Connections

Myasthenia Gravis Induced by Ipilimumab in Patients With Metastatic Melanoma.
Johnson DB, Saranga-Perry V, Lavin PJ, Burnette WB, Clark SW, Uskavitch DR, Wallace DE, Dickson MA, Kudchadkar RR, Sosman JA
(2015) J Clin Oncol 33: e122-4
MeSH Terms: Aged, Antibodies, Monoclonal, Chemotherapy, Adjuvant, Female, Follow-Up Studies, Humans, Ipilimumab, Melanoma, Methylprednisolone, Myasthenia Gravis, Plasmapheresis, Risk Assessment, Sampling Studies, Severity of Illness Index, Skin Neoplasms, Survival Rate, Treatment Outcome
Added June 27, 2014
0 Communities
1 Members
0 Resources
17 MeSH Terms
Expansion of regulatory T cells via IL-2/anti-IL-2 mAb complexes suppresses experimental myasthenia.
Liu R, Zhou Q, La Cava A, Campagnolo DI, Van Kaer L, Shi FD
(2010) Eur J Immunol 40: 1577-89
MeSH Terms: Animals, Antibodies, Monoclonal, Antigen-Antibody Complex, B-Lymphocytes, Cell Separation, Cytokines, Enzyme-Linked Immunosorbent Assay, Female, Flow Cytometry, Interleukin-2, Lymphocyte Activation, Mice, Myasthenia Gravis, Autoimmune, Experimental, T-Lymphocytes, Regulatory
Show Abstract · Added December 10, 2013
Human autoimmune diseases are often characterized by a relative deficiency in CD4(+)CD25(+) regulatory T cells (Treg). We therefore hypothesized that expansion of Treg can ameliorate autoimmune pathology. We tested this hypothesis in an experimental model for autoimmune myasthenia gravis (MG), a B-cell-mediated disease characterized by auto-Ab directed against the acetylcholine receptor within neuromuscular junctions. We showed that injection of immune complexes composed of the cytokine IL-2 and anti-IL-2 mAb (JES6-1A12) induced an effective and sustained expansion of Treg, via peripheral proliferation of CD4(+)CD25(+)Foxp3(+) cells and peripheral conversion of CD4(+)CD25(-)Foxp3(-) cells. The expanded Treg potently suppressed autoreactive T- and B-cell responses to acetylcholine receptor and attenuated the muscular weakness that is characteristic of MG. Thus, IL-2/anti-IL-2 mAb complexes can expand functional Treg in vivo, providing a potential clinical application of this modality for treatment of MG and other autoimmune disorders.
0 Communities
1 Members
0 Resources
14 MeSH Terms
Coexistent autoimmune autonomic ganglionopathy and myasthenia gravis associated with non-small-cell lung cancer.
Peltier AC, Black BK, Raj SR, Donofrio P, Robertson D, Biaggioni I
(2010) Muscle Nerve 41: 416-9
MeSH Terms: Autoimmune Diseases of the Nervous System, Carcinoma, Non-Small-Cell Lung, Electromyography, Ganglia, Autonomic, Humans, Hypotension, Orthostatic, Lung Neoplasms, Male, Middle Aged, Muscle Weakness, Myasthenia Gravis, Norepinephrine, Plasma Exchange, Tachycardia, Treatment Outcome
Show Abstract · Added December 10, 2013
We report the case of a 55-year-old man with non-small-cell lung cancer who underwent radiation, chemotherapy with carbotaxol and paclitaxel, and left upper lobe removal 2 years prior to evaluation. He was referred for disabling orthostatic hypotension (113/69 mm Hg supine and 66/47 mm Hg standing after 10 minutes) without a compensatory heart rate increase (57 to 59 beats per minute), fatigue, and constipation with episodes of ileus. Clinical examination showed mild ptosis bilaterally, fatiguable neck flexor weakness, and hip flexor weakness. Blood pressure response to Valsalva maneuver was abnormal with an absence of phase 4 overshoot and a Valsalva heart rate ratio of 1.04. Plasma norepinephrine level was low (79 pg/ml supine, 330 pg/ml standing). Single-fiber electromyography of the right extensor digitorum communis revealed normal mean consecutive difference (jitter) but several pairs exceeded a jitter of 100 mus. Antibodies against muscle acetylcholine receptor [(AChR) 0.66 nmol/L, normal <0.02 nmol/L] and ganglionic AChR (0.34 nmol/L, normal <0.02 nmol/L) were present. Treatment with plasma exchange normalized responses to standing posture (105/68 supine to 118/82 mm Hg standing, 66 to 79 beats per minute), to Valsalva (normal blood pressure overshoot, hazard ratio 1.47), norepinephrine (194 pg/ml supine, 763 pg/ml standing), and jitter measurements. We conclude that autoimmune autonomic ganglionopathy and myasthenia gravis can coexist and suggest that the latter should be excluded in patients with autoimmune autonomic ganglionopathy who complain of fatigue that shows improvement with non-supine rest.
0 Communities
2 Members
0 Resources
15 MeSH Terms
Natural killer T cells and autoimmune disease.
Wu L, Van Kaer L
(2009) Curr Mol Med 9: 4-14
MeSH Terms: Animals, Arthritis, Rheumatoid, Autoimmune Diseases, Autoimmunity, Diabetes Mellitus, Type 1, Disease Models, Animal, Humans, Immunity, Innate, Immunotherapy, Liver Cirrhosis, Biliary, Lupus Erythematosus, Systemic, Mice, Multiple Sclerosis, Myasthenia Gravis, Natural Killer T-Cells, Self Tolerance
Show Abstract · Added December 10, 2013
Natural killer T (NKT) cells are an unusual subset of innate immune cells that express a surface receptor generated by somatic DNA rearrangement, a hallmark of cells of the adaptive immune system. NKT cells express a highly restricted repertoire of T cell receptors that recognize glycolipid antigens bound with the antigen-presenting molecule CD1d. A hallmark of NKT cells is their capacity to produce copious amounts of immunomodulatory cytokines upon antigenic stimulation, which endows these cells with potent immunoregulatory properties. Consequently, NKT cells have been implicated in regulating a wide variety of immune responses, including immune responses against autoantigens. In patients and mice with a variety of autoimmune diseases, numbers and functions of NKT cells are disturbed, but the relevance of these findings to the etiology of autoimmunity remains to be fully established. Nevertheless, in some mouse models of autoimmunity, NKT cell-deficiency exacerbates disease, suggesting that NKT cells play a role in suppressing autoimmunity. Conversely, specific activation of NKT cells with glycolipid antigens generally protects mice against the development of autoimmunity. Most of these studies have employed the potent sponge-derived NKT cell antigen alpha-galactosylceramide (alpha-GalCer). However, alpha-GalCer treatment in mice was associated with detrimental side effects and treatment efficacy was influenced by a variety of parameters, resulting sometimes in disease exacerbation rather than protection. Recent efforts have focused on developing NKT cell agonists with superior treatment efficacy than alpha-GalCer. Collectively, these studies have identified NKT cells as attractive targets for treatment of human autoimmune diseases.
0 Communities
2 Members
0 Resources
16 MeSH Terms
Cooperation of invariant NKT cells and CD4+CD25+ T regulatory cells in the prevention of autoimmune myasthenia.
Liu R, La Cava A, Bai XF, Jee Y, Price M, Campagnolo DI, Christadoss P, Vollmer TL, Van Kaer L, Shi FD
(2005) J Immunol 175: 7898-904
MeSH Terms: Animals, CD4 Antigens, Female, Forkhead Transcription Factors, Galactosylceramides, Interleukin-2, Killer Cells, Natural, Mice, Mice, Knockout, Myasthenia Gravis, Autoimmune, Experimental, Receptors, Interleukin-2, T-Lymphocytes, Regulatory, Up-Regulation
Show Abstract · Added December 10, 2013
CD1d-restricted NKT cells and CD4+CD25+ regulatory T (Treg) cells are thymus-derived subsets of regulatory T cells that have an important role in the maintenance of self-tolerance. Whether NKT cells and Treg cells cooperate functionally in the regulation of autoimmunity is not known. We have explored this possibility in experimental autoimmune myasthenia gravis (EAMG), an animal model of human myasthenia gravis, induced by immunization of C57BL/6 mice with the autoantigen acetylcholine receptor. We have demonstrated that activation of NKT cells by a synthetic glycolipid agonist of NKT cells, alpha-galactosylceramide (alpha-GalCer), inhibits the development of EAMG. alpha-GalCer administration in EAMG mice increased the size of the Treg cell compartment, and augmented the expression of foxp3 and the potency of CD4+CD25+ cells to inhibit proliferation of autoreactive T cells. Furthermore, alpha-GalCer promoted NKT cells to transcribe the IL-2 gene and produce IL-2 protein. Depletion of CD25+ cells or neutralization of IL-2 reduced the therapeutic effect of alpha-GalCer in this model. Thus, alpha-GalCer-activated NKT cells can induce expansion of CD4+CD25+ Treg cells, which in turn mediate the therapeutic effects of alpha-GalCer in EAMG. Induced cooperation of NKT cells and Treg cells may serve as a superior strategy to treat autoimmune disease.
0 Communities
1 Members
0 Resources
13 MeSH Terms
Natural killer cells determine the outcome of B cell-mediated autoimmunity.
Shi FD, Wang HB, Li H, Hong S, Taniguchi M, Link H, Van Kaer L, Ljunggren HG
(2000) Nat Immunol 1: 245-51
MeSH Terms: Amino Acid Sequence, Animals, Antibody Formation, Autoantibodies, Autoimmunity, B-Lymphocytes, Female, Immunization, Inbreeding, Interferon-gamma, Interleukin-8, Killer Cells, Natural, Lymphocyte Activation, Mice, Mice, Inbred C57BL, Molecular Sequence Data, Myasthenia Gravis, Autoimmune, Experimental, Receptors, Nicotinic, T-Lymphocytes, Torpedo, Transforming Growth Factor beta
Show Abstract · Added December 10, 2013
Natural killer (NK) cells can affect the outcome of adaptive immune responses. NK cells, but not NK1.1+T cells, were found to participate in the development of myasthenia gravis (a T cell-dependent, B cell- and antibody-mediated autoimmune disease) in C57BL/6 mice. The requirement for NK cells was reflected by the lack of a type I helper T cell response and antibodies to the acetylcholine receptor in both NK1.1+ cell-depleted and NK cell-deficient IL-18-/- mice. These findings establish a previously unrecognized link between NK cells and autoreactive T and B cells.
0 Communities
1 Members
0 Resources
21 MeSH Terms