The Immune System Walks a Fine Line
We cannot assume that, as multicellular organisms, our other cell type cannot be foreign to our immune system and so will not be programmed for attack. In fact, our white blood cells, which do the attack, express some different sets of genes from other body cells and logically can attack our own body cells. The fact that this occurs in auto-immune diseases should be the rule rather than the exception, as we are made to believe, (putting aside the adaptation).
What accounts for the apparent tolerance shown by our immune cells to our own cells is an adaptation. There is a similar tolerance shown by our immune system to 'non-disease' causing micro-organisms which inhabit our bowels. Tolerance occurs in gradation. When stimulation of the immune system is low(low dose of microbe) there is no response mounted against 'the foreign'; moderate stimulation leads to T-helper cells activation and attack; higher stimulation results in the weighing in of T-suppressor cells to limit effects which may well spill over to self-cells; still a much higher stimulation(like with self proteins present in high amounts) leads to the death of specific T-helper cell(deletion of the clone) or anergy(loss of co-stimulation for activation). The continuous presence of a 'foreign cell protein' in the vicinity of our immune cells such as our other cells and microbes that invade and colonize our bowels will be subject to this gradation in function.
Of special mention are the super-antigens, like bacterial lipopolysaccharides and allogenous antigens, that cross-bind and lock the major histocompatibility complex(MHCII), also known as HLA(human leucocyte antigen), but do not do so classically as processed antigens by macrophages and this results in the production of polyclonal antibodies that aggressively attack practically all body cells. This leads to inflammation, as specific immunity is staved, and explains how staph and strep toxins work and produce anergy. By preventing the phagocytes from binding to the Tc of the antibody, staphs and streps will force these phagocytes to produce pyogenic inflammation, through toxic leukocidins.
B-anergy will occur on exposure of soluble antigen with some loss of IgM expression.
Whatever illness a non-toxin-producing microbe, an innocuous allogenous substance or the 'altered self 'will cause, will be the result of our innate or adaptive immune malfunction, above and below the norm.
Dr Oliver Verbe Birnso.M.D.
What accounts for the apparent tolerance shown by our immune cells to our own cells is an adaptation. There is a similar tolerance shown by our immune system to 'non-disease' causing micro-organisms which inhabit our bowels. Tolerance occurs in gradation. When stimulation of the immune system is low(low dose of microbe) there is no response mounted against 'the foreign'; moderate stimulation leads to T-helper cells activation and attack; higher stimulation results in the weighing in of T-suppressor cells to limit effects which may well spill over to self-cells; still a much higher stimulation(like with self proteins present in high amounts) leads to the death of specific T-helper cell(deletion of the clone) or anergy(loss of co-stimulation for activation). The continuous presence of a 'foreign cell protein' in the vicinity of our immune cells such as our other cells and microbes that invade and colonize our bowels will be subject to this gradation in function.
Of special mention are the super-antigens, like bacterial lipopolysaccharides and allogenous antigens, that cross-bind and lock the major histocompatibility complex(MHCII), also known as HLA(human leucocyte antigen), but do not do so classically as processed antigens by macrophages and this results in the production of polyclonal antibodies that aggressively attack practically all body cells. This leads to inflammation, as specific immunity is staved, and explains how staph and strep toxins work and produce anergy. By preventing the phagocytes from binding to the Tc of the antibody, staphs and streps will force these phagocytes to produce pyogenic inflammation, through toxic leukocidins.
B-anergy will occur on exposure of soluble antigen with some loss of IgM expression.
Whatever illness a non-toxin-producing microbe, an innocuous allogenous substance or the 'altered self 'will cause, will be the result of our innate or adaptive immune malfunction, above and below the norm.
Dr Oliver Verbe Birnso.M.D.
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