Immune reactions, types

Contamination of blood products with lymphocytes can lead to transfusion-induced reactions ranging from a mild fever to severe reactions such as alloimmunization and graft versus host disease (GvHD), in which the transfused lymphocytes (graft) survive the defensive immune reaction of the patient (host) and start a reaction which destroys the cells of the host. The patient also may develop an immune response to the human leukocyte antigen (HLA) type of the graft s cells and reject all platelet transfusions that do not match their own HLA system. The HLA system, found on blood platelets and lymphocytes, is more compHcated than, but similar to, the ABO blood group system of red cells. 

Now consider a latticized version of this model. Populate a square lattice -which may represent a tissue sample in which the modeled immune reactions are assumed to occur - with each of the four cell types C, H, M and V and initialize the system so that a fraction po of each cell type is in its high (i.e. = 1) concentration state. Assign the value 1 to each site i,j) if the sum of the concentrations of its nearest neighbors that are of the same cell type as site (i, j) is nonzero. After all sites have been assigned new values in this manner, update the system according to equations 8.92. 

Currently allergic reactions are classified into four types on the basis of different reaction patterns. Whereas types I—III are dependent on antibodies, the type IV reaction is mediated by cellular immune reactions. 

Delayed type hypersensitivty (DTH) reactions (synonym type IV allergic reactions) are exaggerated, T-lymphocyte mediated, cellular immune reactions to foreign substances, which require one to two days to manifest clinical symptoms. 

Most anaphylactoid reactions are due to a direct or chemical release of histamine, and other mediators, from mast cells and basophils. Immune-mediated hypersensitivity reactions have been classified as types I-IV. Type I, involving IgE or IgG antibodies, is the main mechanism involved in most anaphylactic or immediate hypersensitivity reactions to anaesthetic drugs. Type II, also known as antibody-dependent hypersensitivity or cytotoxic reactions are, for example, responsible for ABO-incompatible blood transfusion reactions. Type III, immune complex reactions, include classic serum sickness. Type IV, cellular responses mediated by sensitised lymphocytes, may account for as much as 80% of allergic reactions to local anaesthetic. 

The newer derivatives seem less likely to cause hypersensitivity reactions, perhaps because the protein adducts generated are shorter lived. All four types of hypersensitivity reaction have been observed with penicillin. Thus, high doses may cause hemolytic anemia and immune complex disease and cell-mediated immunity may give rise to skin rashes and eruptions, and the most common reactions are urticaria, skin eruptions, and arthralgia. Antipenicillin IgE antibodies have been detected consistently with an anaphylactic reaction. The anaphylactic reactions (type 1 see above), which occur in 0.004% to 0.015% of patients, may be life threatening. 

There are thus various autoantibodies present, and if the auto-antigens are released by cellular breakdown, a type III immune reaction can occur where an immune complex is formed, which is deposited in small blood vessels and joints, giving rise to many of the symptoms. The immunoglobulins IgG and IgE act as both autoantibody and antigen, and hence immune complexes form. Such complexes stimulate the complement system leading to inflammation, infiltration by polymorphs and macrophages, and the release of lysosomal enzymes. 

This is a vasodilator drug, which causes SLE in a significant proportion of patients. Several predisposing factors have been identified dose (>25 mg) duration of therapy (mean 18 months) acetylator phenotype (slow) HLA type (DR4) and gender (females males, 4 1). Antinuclear antibodies and antihydralazine antibodies are detected in serum. This causes a type III immune reaction. Mechanism is unclear but may involve interference with the development and maturation of T cells in the thymus, leading to an alteration of tolerance... 

Heparin-induced thrombocytopenia (HIT) can likewise be asymptomatic and resolve spontaneously (type I HIT), or it can be severe (type II HIT). Type II HIT is mediated by an immune reaction, which can lead to serious complications including increased thrombosis in vascular tissues throughout the... 

Other problems that may be encountered are related to the immunologic effects of insulin use. Certain forms of insulin may evoke an immune reaction and stimulate antibody production. These anti-insulin antibodies may cause an allergic reaction in some individuals, as well as a resistance to the exogenous insulin molecule. As discussed previously, the incidence of these immunologic reactions seems to be greater when animal (i.e., pork) forms of insulin are used. Consequently, these problems are often resolved by switching the patient to another type of preparation, preferably biosynthetic human insulin. 

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