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Multiple Autoimmunity

In December 1991, a project team was formed to develop fhe anfi-CD20 antibody. Acfually, two teams were formed at the same time, one to lead the development of anfi-CD4 and fhe ofher to lead fhe developmenf of anfi-CD20. Anfi-CD4, an antibody fhaf affecfs helper T cells, was fhought to have incredible potential to affect multiple autoimmune diseases, which were thought to be dependent on helper T cells. The autoimmune diseases included rheumatoid arthritis, and possibly, allergic asthma — both diseases with enormous markets and without effective treatmenf options. A nondeplefing modified version of fhe anfi-CD4 monoclonal antibody was still under consideration for additional clinical frials in 2005. [Pg.575]

In addition to cancer, too little apoptosis can also result in diseases such as autoimmune lymphoproliferative syndrome (ALPS). This occurs when there is insufficient apoptosis of auto-aggressive T cells, resulting in multiple autoimmune diseases. An overproliferation of B cells occurs as well, resulting in excess immunoglobulin production, leading to autoimmunity. Some of the common diseases of ALPS include hemolytic anemia, immune-mediated thrombocytopenia, and autoimmune neutropenia. The different types of this condition are caused by different mutations. Type 1A results from a mutation in the death domain of the Fas receptor, Type IB results from a mutation in Fas ligand, and Type 2 results from a mutation in caspase 10, reducing its activity. [Pg.312]

One lineage choice that occurs rather late in T-cell ontogeny is the development of NKT cells. NKT cells express markers of both NK cells and T lymphocytes. These include Ly49 family receptors NKl.l and TCR in mice. Mature NKT cells are CD44 CD69, a phenotype consistent with an activated cell. A hallmark of NKT cells is copious IL-4 and IFN-y secretion promptly upon TCR activation. Because of this property, NKT cells most Likely possess regulatory fimctions. They suppress multiple autoimmune phenomena, and in some cases, inhibit tumor metastases. Unlike conventional a 3 T cells that are selected by classical MHC class I and II, the vast majority of NKT cells are selected by the non-polymoiphic class I-like molecule, CD Id. [Pg.140]

Hafler JP, Maier LM, Cooper JD, Plagnol V, Hinks A, Simmonds MJ et al (2009) CD226 Gly307Ser association with multiple autoimmune diseases. Genes Immun 10 5-10... [Pg.658]

Animal models suggest that both genetic and environmental factors are important in co-morbidity, and of particular interest is the way in which environmental factors can modify genetic susceptibility. Thus, non-obese diabetic (NOD) mice develop thyroiditis and sialo-adenitis in addition to autoimmune diabetes (Skarstein et al., 1995). This expression of autoimmune disorders is modified by the degree of microbial contamination of the environment (Rossini et al., 1995) and by early life exposure to filarial worms (Imai et al., 2001). In both cases, early immune stimulation leads to lower incidence of diabetes, showing how genetic susceptibility to multiple autoimmune disorders may be disguised by environmental factors. [Pg.91]

Fig. 6 Rituximab literature reports (autoimmune diseases). The indications and clinical applications for rituximab are expanding as research in the therapy of multiple autoimmune diseases is reported. This list is a sample of the literature reports on the many indications currently under investigation. Fig. 6 Rituximab literature reports (autoimmune diseases). The indications and clinical applications for rituximab are expanding as research in the therapy of multiple autoimmune diseases is reported. This list is a sample of the literature reports on the many indications currently under investigation.
Brown RJ, Rother KI, Artman H, Mercuric MG, Wang R, Looney RJ, Cowen EW. Minocycline-induced drug hypersensitivity syndrome followed by multiple autoimmune sequelae. Arch Dermatol 2009 145(1) 63-6. [Pg.508]

Transfusion-induced autoimmune disease has been a significant complication in the treatment of patients who require multiple platelet transfusions. Platelets and lymphocytes carry their own blood group system, ie, the human leukocyte antigen (HLA) system, and it can be difficult to find an HLA matched donor. A mismatched platelet transfusion does not induce immediate adverse reactions, but may cause the patient to become refractory to the HLA type of the transfused platelets. The next time platelets with an HLA type similar to that of the transfused platelets are transfused, they are rejected by the patient and thus have no clinical efficacy. Exposure to platelets originating from different donors is minimized by the use of apheresis platelets. One transfusable dose (unit) of apheresis platelets contains 3-5 x 10 platelets. An equal dose of platelets from whole blood donation requires platelets from six to eight units of whole blood. Furthermore, platelets can be donated every 10 days, versus 10 weeks for whole blood donations. [Pg.520]

For the pathogenesis of multiple sklerosis, autoimmune T-lymphocy tes play a predominant role, which are directed against components of the neural myelin sheath. T-lymphocy tes by secreting cytokines such as interferon y maintain the chronic inflammation which destructs the myelin sheath. Also cytotoxic T-lymphocytes may participate directly. The cause of multiple sklerosis is unknown. Significantly increased antibody titers against several vitusses, mostly the measles virus, point to a (latent) virus infection initiating the disease. [Pg.241]

Interferon beta-la (AVONEX , Rebif ), interferon beta-lb (Betaferon ), and interferon beta (Fiblaferon ) are applied in multiple sclerosis to reduce both frequency and severity of disease incidents and for the treatment of severe viral infections. In multiple sclerosis, DFN- 3 proteins modulate the destruction of myelin in the cause of the autoimmune reaction. [Pg.411]

Multiple scelerosis is an autoimmune disease mediated by T and B lymphocytes and macrophages. This is characterized by extensive inflammation and demyelination of the myelin sheath that surrounds the nerve fiber. The death of the nerve fiber results in a variety of symptoms that can lead to impairment of movement, paralysis, and death. [Pg.794]

American co net lower, black susans) angustifolia shortens symptoms and duration of upper respiratory Infections (URIs) including colds mild gastrointestinal (Gl) upsets individuals with autoimmune diseases such as tuberculosis, collagenosis, multiple sclerosis, AIDS and HIV infection. [Pg.659]

Hibbs ML, Tarlinton DM. Armes J. Grail D. Hodgson G, Maghtto R, Stacker SA, Dunn AR Multiple defects in the immune system of Lyn-deficient mice, culminating in autoimmune disease. Cell 1995 83 301-311. Nishizumi H, Yamamoto T Impaired tyrosine phosphorylation and Ca + mobiUzation, but not degranulation, in Lyn-deficient bone marrow-derived mast cells. J Immunol 1997 158 2350-2355. [Pg.65]

CCR5 expression likely plays a role in T-cell recruitment and may be involved in the development of autoimmune diseases. There is a negative association between the CCR5A32 mutation and rheumatoid arthritis (Prahalad 2006). Furthermore, additional studies reviewed elsewhere suggest the involvement of CCR5 in multiple sclerosis, diabetes, and transplant rejection (Ribeiro and Horuk 2005). As such, it is likely that CCR5 antagonists developed for the treatment of HIV-1 infection can also be used for other diseases. [Pg.43]

EAE experimental autoimmune encephalomyehtis, MHVmmmt hepatitis virus, LCMVlymphocytic choriomeningitis virus, MS multiple sclerosis, IWWWest Nile virus, TBEVtick-borne encephalitis virus... [Pg.123]

McCandless EE, Wang Q, Woerner BM, Harper JM, Klein RS (2006) CXCL12 Umits inflammation by localizing mononuclear infiltrates to the perivascular space during experimental autoimmune encephalomyelitis. J Immunol 177 8053-8064 McCandless EE, Piccio L, Woerner BM, Schmidt RE, Rubin JB, Cross AH, Klein RS (2008a) Pathologic expression of CXCL12 at the blood brain barrier correlates with severity of multiple sclerosis. Am J Pathol... [Pg.141]

McCandless EE, Budde M, Lees JR, Dorsey D, Lyng E, Klein RS (2009) IL-IR signaling within the central nervous system regulates CXCL12 expression at the blood-brain barrier and disease severity during experimental autoimmune encephalomyehtis. J Immunol 183(l) 613-620 McEarland HE, Martin R (2007) Multiple sclerosis a complicated picture of autoimmunity. Nat Immunol 8 913-919... [Pg.142]

Cyclosporine and tacrolimus are calcineurin inhibitors that are administered as part of immunosuppressive regimens in kidney, liver, heart, lung, and bone marrow transplant recipients. In addition, they are used in autoimmune disorders such as psoriasis and multiple sclerosis. The pathophysiologic mechanism for ARF is renal vascular vasoconstriction.41 It often occurs within the first 6 to 12 months of treatment, and can be reversible with dose reduction or drug discontinuation. Risk factors include high dose, elevated trough blood concentrations, increased age, and concomitant therapy with other nephrotoxic drugs.41 Cyclosporine and tacrolimus are extensively metabolized by... [Pg.370]

Some aspects of multiple sclerosis are reflected in the animal model experimental autoimmune encephalomyelitis, which is induced by immunization of susceptible animals with appropriate encephalogenic proteins or peptides. In these animals, if cultured adult stem cell neurospheres are injected into the bloodstream, injected cells can find their way to damaged portions of the nervous system and improve function in mice. How the injected cells augmented the recovery process is unclear. One possibility is that cells recruited to the lesions differentiated into oligodendrocytes and generated new myelin sheaths, but this seems unlikely in the face of ongoing cellular destruction. [Pg.512]

Iglesias, A., Bauer, J., Litzenburger, T. etal. T- and B-cell responses to myelin oligodendrocyte glycoprotein in experimental autoimmune encephalomyelitis and multiple sclerosis. Glia 36 220-234,2001. [Pg.651]

Fast-channel syndrome. The clinical features resemble those of autoimmune myasthenia gravis (see below) with variable severity. Conversely to what is found in slow-channel syndrome, the open state of the AChR is destabilized, manifesting as fast dissociation of ACh from the receptor and/or excessively reduced open times. One mutation has also caused multiple congenital joint contractures owing to fetal hypomotility in utero. In most cases, the mutant allele causing the kinetic abnormality... [Pg.720]


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Autoimmune

Autoimmunization

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