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causes of cell injury
causes of cell injury

... This is vital for coordinating complex activities such as growth, adaptation and other responses to both intrinsic and extrinsic stimuli. There are numerous chemical messengers that facilitate this process including various classes of growth factors and immune modulators. ...
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Abstract:
Abstract:

... decreased survival. The increased pathogenicity in T. brucei infected mice correlated with uncontrolled IFN- production, marginal IL-10 production and continuous stimulation of classically activated monocytic cells (M1), producing the pathogenic molecules TNF- and NO. Conversely, the decreased pat ...
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Severe Combined Immune Deficiency (SCID)
Severe Combined Immune Deficiency (SCID)

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First line of defense - CGW-Life-Science
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Cancer Immunity: Lessons From Infectious

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Trine R Thomsen1,2*, Xu1,2, Lone Heimann Larsen1,3,

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Responder Individuality in Red Blood Cell Alloimmunization

... matched blood, in the process of alloimmunization. Alloimmunization may or may not occur in individuals exposed to ‘non-self’ blood group antigens. Many researchers have intensively studied the variables that determine the process of blood group alloimmunization. However, to date, there are only som ...
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... to CD4+ T cells. They also play a role in the selection of the TCR repertoire in the thymus. Because CD4+ T cells recognize linear stretches of about 9–20 amino acids derived from self or foreign protein antigens bound in the peptide-binding groove of polymorphic MHC class II molecules, it has been ...
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... – The key to do this is recognition of what does belong in your body, or what is “self” vs. what does not belong in the body, or what is “foreign” (not self). – All “self” cells have a recognizable complement of surface markers – Foreign cells and structures have non-self markers which are capable o ...
Comparison of the immune response elicited by infectious and
Comparison of the immune response elicited by infectious and

< 1 ... 272 273 274 275 276 277 278 279 280 ... 514 >

Molecular mimicry

Molecular mimicry is defined as the theoretical possibility that sequence similarities between foreign and self-peptides are sufficient to result in the cross-activation of autoreactive T or B cells by pathogen-derived peptides. Despite the promiscuity of several peptide sequences which can be both foreign and self in nature, a single antibody or TCR (T cell receptor) can be activated by even a few crucial residues which stresses the importance of structural homology in the theory of molecular mimicry. Upon the activation of B or T cells, it is believed that these ""peptide mimic"" specific T or B cells can cross-react with self-epitopes, thus leading to tissue pathology (autoimmunity). Molecular mimicry is a phenomenon that has been just recently discovered as one of several ways in which autoimmunity can be evoked. A molecular mimicking event is, however, more than an epiphenomenon despite its low statistical probability of occurring and these events have serious implications in the onset of many human autoimmune disorders. In the past decade the study of autoimmunity, the failure to recognize self antigens as ""self,"" has grown immensely. Autoimmunity is a result of a loss of immunological tolerance, the ability for an individual to discriminate between self and non-self. Growth in the field of autoimmunity has resulted in more and more frequent diagnosis of autoimmune diseases. Consequently, recent data show that autoimmune diseases affect approximately 1 in 31 people within the general population. Growth has also led to a greater characterization of what autoimmunity is and how it can be studied and treated. With an increased amount of research, there has been tremendous growth in the study of the several different ways in which autoimmunity can occur, one of which is molecular mimicry. The mechanism by which pathogens have evolved, or obtained by chance, similar amino acid sequences or the homologous three-dimensional crystal structure of immunodominant epitopes remains a mystery.
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