Sandbox:AA: Difference between revisions
Aysha Aslam (talk | contribs) No edit summary |
Aysha Aslam (talk | contribs) No edit summary |
||
| Line 30: | Line 30: | ||
| F || Incidence || Prevalence | | F || Incidence || Prevalence | ||
|} | |} | ||
[[Atopic/anaphylactic (HIR) Type I IgE, mast cells Urticaria, Hives, Asthma Unknown | |||
Neutralization (HIR) IgG Endotoxin neutralization: diptheria, tetanus, cholera, etc. Unknown | |||
Cytotoxic/cytolytic (HIR) Type II IgM, IgG, complement, (agglutination, lysis opsonization) Transfusion reactions, Goodpasture syndrome, Pemphigus Unknown | |||
Immune Complex (Arthus) reaction (HIR) Type III IgG, IgA, and/or IgM antibody-antigen complexes, neutrophils, complement Cutaneous leukocytoclastic vasculitis, Arthus reaction, serum sickness, glomerulonephritis. Acute inflammatory response | |||
Cellular cytotoxic CD8 T-cells, natural killer cells Lichen planus, graft-versus-host disease Not clear (T. pallidum is not, per se, an intracellular pathogen) | |||
Delayed Type Hypersensitivity (DTH) Type IV CD4 T-cells, cytokines, Activated macrophages Destruction of infected macrophages in tuberculosis and leprosy; positive tuberculin test Activated macrophages destroy T. pallidum | |||
Granulomatous reactions* Macrophages, lymphocytes Foreign body granuloma, isolation of organisms in granulomas of leprosy, tuberculosis, syphilis Possible reaction to persistent T. pallidum cell wall antigens]] | |||
[These clinical stages, in turn, reflect the interaction of the infectious agent with the host, and the effects of the immune response on the infection. Of particular importance is the strength of delayed type hypersensitivity (DTH), which is mediated by CD4+ cells. Humoral antibody or CD8+ cytotoxic T-cells (TCTL) are relatively ineffective in clearing syphilitic infections, or in controlling progression of lesions; secondary and tertiary disease ensue if the DTH response is insufficiently effective.Throughout this review, DTH will refer to a beneficial cell mediated immune host response characterized by an expanded population of antigen specific T cells that produce cytokines locally, activating and recruiting additional lymphocytes and macrophages (9). Macrophages accumulate at the site of DTH and become activated through the CD4 Th1 cell-cytokine-macrophage interactions protecting against infection by destroying and clearing the organism. However, high, persistent localized antigenic challenge can lead to excessive and/or chronic inflammatory response producing immunopathology in the form of granulomatous inflammation, tissue destruction, and the formation of secondary lymphoid organs (e.g. lymphoid follicles and plasma cell infiltrates) (9, 10). In this setting, granulomas are believed to form as a result of the persistence of non-degradable (non-replicative) infectious antigen.] | |||
Revision as of 19:51, 20 September 2016
Aysha's sandbox
| Region | Gender | Incidence/100,000 | Prevalence/100,000 |
|---|---|---|---|
| Region 1 | M | Incidence | Prevalence |
| F | Incidence | Prevalence | |
| Region 2 | M | Incidence | Prevalence |
| F | Incidence | Prevalence | |
| Region 3 | M | Incidence | Prevalence |
| F | Incidence | Prevalence | |
| Region 4 | M | Incidence | Prevalence |
| F | Incidence | Prevalence | |
| Region 5 | M | Incidence | Prevalence |
| F | Incidence | Prevalence |
[[Atopic/anaphylactic (HIR) Type I IgE, mast cells Urticaria, Hives, Asthma Unknown Neutralization (HIR) IgG Endotoxin neutralization: diptheria, tetanus, cholera, etc. Unknown Cytotoxic/cytolytic (HIR) Type II IgM, IgG, complement, (agglutination, lysis opsonization) Transfusion reactions, Goodpasture syndrome, Pemphigus Unknown Immune Complex (Arthus) reaction (HIR) Type III IgG, IgA, and/or IgM antibody-antigen complexes, neutrophils, complement Cutaneous leukocytoclastic vasculitis, Arthus reaction, serum sickness, glomerulonephritis. Acute inflammatory response Cellular cytotoxic CD8 T-cells, natural killer cells Lichen planus, graft-versus-host disease Not clear (T. pallidum is not, per se, an intracellular pathogen) Delayed Type Hypersensitivity (DTH) Type IV CD4 T-cells, cytokines, Activated macrophages Destruction of infected macrophages in tuberculosis and leprosy; positive tuberculin test Activated macrophages destroy T. pallidum Granulomatous reactions* Macrophages, lymphocytes Foreign body granuloma, isolation of organisms in granulomas of leprosy, tuberculosis, syphilis Possible reaction to persistent T. pallidum cell wall antigens]]
[These clinical stages, in turn, reflect the interaction of the infectious agent with the host, and the effects of the immune response on the infection. Of particular importance is the strength of delayed type hypersensitivity (DTH), which is mediated by CD4+ cells. Humoral antibody or CD8+ cytotoxic T-cells (TCTL) are relatively ineffective in clearing syphilitic infections, or in controlling progression of lesions; secondary and tertiary disease ensue if the DTH response is insufficiently effective.Throughout this review, DTH will refer to a beneficial cell mediated immune host response characterized by an expanded population of antigen specific T cells that produce cytokines locally, activating and recruiting additional lymphocytes and macrophages (9). Macrophages accumulate at the site of DTH and become activated through the CD4 Th1 cell-cytokine-macrophage interactions protecting against infection by destroying and clearing the organism. However, high, persistent localized antigenic challenge can lead to excessive and/or chronic inflammatory response producing immunopathology in the form of granulomatous inflammation, tissue destruction, and the formation of secondary lymphoid organs (e.g. lymphoid follicles and plasma cell infiltrates) (9, 10). In this setting, granulomas are believed to form as a result of the persistence of non-degradable (non-replicative) infectious antigen.]