Term
| Two Phases of Hypersensitivity Reactions |
|
Definition
Sensitization Phase Pathological Phase (the rxn itself) |
|
|
Term
|
Definition
| Type I is where you have the presence of specific IgE antibodies against a particular allergen. So the sensitization phase here is that an individual acquires an allergen, raises IgE antibodies against that allergen following exactly the same processes that we’ve discussed about how Ab is formed and IgE Ab is made against that allergen. And so, these IgE antibodies will bind to the IgE Fc receptors on the surface of mast cells. Then if that individual encounters this allergen again, that allergen may bind to IgE Ab molecules on the surface of the mast cell. A key requirement here again is that it has to have cross-linked IgE antibodies, so there has to be two or more adjacent IgE Ab molecules that can bind to the same allergen, providing this cross-linking aspect to it, before the mast cell can become activated and degranulate releasing the granule contents which are histamine and serotonin and several other vasoactive amines. |
|
|
Term
|
Definition
| Type II hypersensitivity is also called Ab-mediated or cytotoxic hypersensitivity reaction. A target cell has to be present that has epitopes on its surface that can stimulate the production of antibodies, typically IgG antibodies. There’s at least two different ways that this pathology can be elicited here or be seen here. So, the first phase or the sensitization phase is induction of the antibodies against the target antigens and the second phase is when the individual encounters that particular target cell again coated with these particular foreign epitopes on the surface and IgG Ab can bind to those foreign epitopes on the surface of the target cell. And then, cells involved in the cell-mediated response, shown here as the killer T cell, can also have an NK cell here as well, that have Fc receptors on their suface binding to the Fc region of the IgG. Then there is the release of perforins and granzymes and other lysis causing molecules that can destroy this target cell. An alternative mechanism is where there is activation of the complement system, in this case what is shown here is Ab-mediated so this would be a classical complement activation pathway where Ab can bind and C1 can bind two or more adjacent Ab molecules…(inaudible)…and then there would be lysis of this target cell. |
|
|
Term
| Type III Hypersensitivity |
|
Definition
| Type III hypersensitivity reaction is also called immune-complex reaction. The first step or sensitization phase is when there is induction of an Ab response against the antigen, in this case the antigen has to be a soluble antigen, must be a soluble antigen. Most common isotype is IgG, so there’s induction of IgG antibodies against these soluble antigens. Subsequent exposure will lead to essentially precipitation of the soluble antigen with Ab molecules, and it will be agglutination of those soluble antigens binding to the surface of endothelial cells or simply occluding those capillaries, blocking passage of red blood cells and white blood cells through the capillary. There can be activation of the complement system or there can be phagocytic cells that have Fc receptors on their surface binding to the Fc region of these Ab molecules. The end result is that there is destruction of the adjacent tissue, in this case the endothelial cells lining the blood vessel walls. So the neutrophils may bind, for example, via the Fc receptors, the neutrophils may engulf this complex and lyse the neutrophil, releasing its intracellular contents that contain all of those proteolytic enzymes that will degrade and destroy these endothelial cells. The complement system may also be activated and try to destroy this complex. In reality, what it may do is lyse the patient’s own endothelial cells causing pathology there as well. |
|
|
Term
|
Definition
| Type IV or delayed-type hypersensitivity, the first step is the passage of the allergen typically through the skin and acquisition of that allergen by antigen-presenting cells, such as Langerhan cells. Those Langerhan cells then pass that antigen typically to lymph nodes where there is activation of T cells and the induction of memory T cells. Upon subsequent exposure of that allergen to this individual, those allergens can encounter these memory T cells, releasing large amounts of cytokines causing the recruitment of inflammatory cells, including activated macrophages which will in turn release more inflammatory cytokines such as IL-1 or TNF-alpha, causing additional recruitment of inflammatory cells to that site. |
|
|
Term
|
Definition
Type I hypersensitivity to natural rubber latex proteins Reaction may include nose, eyes, and skin reactions More serious reactions may include respiratory distress--rarely shock or death |
|
|
Term
|
Definition
Irritant contact dermatitis - Not an allergy (not a true hypersensitivity reaction)
- Dry, itchy, irritated areas
Allergic contact dermatitis - Type IV delayed hypersensitivity
- May result from allergy to chemicals used in glove manufacturing
|
|
|
Term
|
Definition
|
|
