Failures of Host Defense Mechanism
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butterfly121278 on November 18, 2010
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Terms | Definitions |
|---|---|
 Evasion of immune responses | •Mechanisms -Antigenic variation (between serotypes) (12-1) -Antigenic variation (by changing gene expression) (12-1) -Antigenic drift (12-1) -Antigenic shift (12-1) -Latency (of viruses) (12-2) |
| Evading the immune system with antigenic variation | •S. pneumoniae makes a wide variety of capsule polysaccharides within the species, therefore immunological memory to one serotype does not confer immunity to all •Common cause of bacterial pneumonia |
| Trypansomes | can change genes for surface antigens |
| Antigenic drift | mutations in antigens lead to virus that is not recognized |
| Antigenic shift | recombination of viral genes and therefore antigens in a cell infected with two strains of a virus |
| Latent viruses integrate into host's genome | •Reactivation: de-integrates and begins replication •Epithelial cells killed by cytotoxic T-cells, but neurons produce low levels of MHC I and escape •Examples: -Herpes simplex -Herpes zoster -EBV |
| Subversion of immune response (12-3) | •M. tuberculosis prevents formation of phagolysosome in a macrophage •L. monocytogenes breaks out of phagolysosome •T. pallidum (syphilis) coats itself with human proteins •Viruses have many strategies -Turn off MHC I and/or TAP -Make proteins that inhibit complement -Alter cytokine production |
| Suppression of immunity through overactivation of the immune system: superantigens (12-4) | •Cause CD4+ T-cells to bind MHC II that they normally wouldn't •Massive non-specific T-cell activation |
| Primary (genetic) Immunodeficiency diseases | •Range from severe to minor decrease in immunity •Mutation in genes for various proteins- But there is redundancy in the system - mutation does not necessarily lead to disease •Loss of different components leads to different symptoms (12-7) -Defects in antibodies, complement, or phagocytosis lead to infection with pyogenic bacteria -Defect in T cells often leads to fungal infections |
| Antibody deficiencies (12-9 to 12-10) | •X-Linked Agammaglobulinema (XLA): mutation in kinase needed for signaling in B cells •X-linked hyper IgM syndrome: Mutation of CD40L •AID deficiency -No isotype switching and little somatic hypermutation -Causes hyper IgM syndrome •Transient antibody deficiency occurs in normal babies |
| X-linked agammaglobulinemia (XLA) | •Missing protein that is part of signal from B-cell receptor that antigen has been bound •No antibodies •Pre-B-cells with defective gene fail to develop to naïve stage |
| X-Linked Hyper-IgM syndrome | •Mutation in CD40L (on T cells) -No germinal centers in lymph nodes, so no isotype switching |
| Transient antibody deficiency in normal infants | •Infant is born with mother's IgG, but this wears off •3 months to 1 yr, IgG, IgE, and IgA (if not breastfed) are low |
| Complement deficiencies (12-11) | •Mutations up to and including C3 cause susceptibility to pyogenic bacteria. Normally opsonization helps to clear these •Mutations in membrane attack complex lead to increased risk of infection with Neisseria bacteria |
| Defects in phagocytic cells (12-12) | •Deficiency of neutrophils is fatal unless treated •Leukocyte adhesion deficiency - mutant cell adhesion molecule, therefore phagocytes can't stick and migrate to infected tissue •Chronic granulomatous disease - phagocytes can't make toxic oxygen molecules, leading to granulomas (clusters of infected macrophages walled off from the rest of the tissue) |
| Lack of functional T-cells leads to SCID (severe combined immunodeficiency) | •X-linked SCID -Mutation in protein shared by many, therefore missing receptors for IL-2, IL-4, IL-7 and other cytokines needed for T-cell activation and growth •RAG deficiency also causes SCID |
| Treating immunodeficiency diseases 12-15 | •Bone marrow transplantation -Marrow from a donor has stem cells with different genome -Donor and recipient must be at least partial MHC match (top) -Donor's T cells are selected in the recipient's thymus and therefore recognize only recipient's MHCs (middle) -APCs are from donor, so only MHCs that are common to donor and recipient can present antigen (bottom) |
| Problems with bone marrow transplant 12-16 | •Naïve T cells that have been selected against the donor's MHC can become activated against host's cells (graft vs. host disease) -Now T cells can be removed before putting the bone marrow into host •Host's naïve T cells that have not been selected against the donor's MHC can become activated against donor's stem cells (graft failure or host vs. graft disease) -To prevent this, the host's immune system is usually destroyed before the transplant |
| HIV / AIDS: A secondary (non-genetic) immunodeficiency disease | •HIV is the pathogen; AIDS is the disease |
| AIDS - clinical observations | •Low CD4 T cell count -Without helper T cells, other components of the immune system are not activated •High rate of infection and/or cancer (Kaposi's sarcoma or B-cell cancer) |
| HIV structure | • Retrovirus (RNA genome that must be reverse transcribed into DNA)• Surrounding genome is a protein shell, and surrounding that is a phospholipid bilayer with gp120 proteins in it. |
| HIV infection | •1. virus binds CD4 and co-receptor on T-cell, which triggers fusion of viral membrane with cell's plasma membrane •Three cell types have CD4 on surface -CD4+ T-cells -Macrophages -Dendritic cells -Infection of phagocytes tends to spread infection; infection of T cells tends to kill host |
| HIV entry details 12-21 | •gp120 binds to CD4 plus one of two co-receptors -CCR5 on macrophages and DCs •In infection through mucus membranes, this variety is most common in initial infection -CXCR4 on activated T cells -Virus can be specific for one or the other or both |
| HIV infection | •2. Reverse transcriptase makes DNA copy of RNA genome •3. DNA integrates into host cell's genome •4. When T-cell becomes activated, transcription begins. mRNA is spliced to make early proteins Tat and Rev •5. Early proteins amplify transcription and turn on expression of all proteins •6. New virus buds from cell |
| Typical time course of infection | •Infected people can remain asymptomatic for many years. Symptoms begin when CD4 T-cell count drops below certain level. |
| A few people seem resistant | •Some seem to be able to keep it at low levels through immune activity •Some lack CCR5 co-receptor (the one needed to spread the infection) and therefore do not contract virus |
| First wave of anti-HIV drugs -- protease inhibitors | •High rate of mutation of virus led to rapid resistance |
| Highly active antiretroviral therapy (HAART) | •Combination therapy- typically three or four drugs - has a synergistic effect and keeps viral load low enough that it can't develop resistance |
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