Chapter 5: Diseases of the immune system
The adaptive immune system comes with its limitations. There are 3 typical immune
reactions with negative effects:
1. Hypersensitivity type I-IV
2. Unwanted immune reactions, like auto-immune or transplant rejections
3. Decreased immunity, due to immunodeficiencies.
Short recap immunology:
B lymphocytes become antibodies; Ig gene editing via 2 phases. Phase 1 is random, before
contact with the antigen happens in the bone marrow. Phase 2 is non random, occurs after
contact antigen to make it perfectly suitable, happens in the lymph nodes.
T lymphocytes become effector T cells. The CD4+ T cells bind antigen though their TCR that
is presented via MHC type 2. Become other t cells or memory t cells. Always an extracellular
antigen which is processed. The CD8+ T cell bind antigen via other TCR that is presented in
MHC type 1, always intracellular so mostly viruses.
1. Hypersensitivity
Type 1: allergy; upon activation of TH2 cells, IgE production starts. Binds to mast cells. Can
be an immediate hypersensitivity reaction (minutes) or late reaction (after repeated
exposure). Eosinophils are super active in allergy.
Type 2: antibody mediated; tissue damage or dysfunction due to antibodies binding to
receptors. Example is pemphigus vulgaris, antibodies against epidermal intercellular
adhesion molecule. Example is Graves’ disease, where the antibody bind to the TSH
receptor, constant thyrohyoid hormone secretion, hypermetabolic state. Example is
Myasthenia Gravis, antibody inhibits activation ACh recptor, less muscle activation.
Type 3: immune complex mediated; antigen-antibody complex, binding the vessel wall
causing further damage and induce phagocytosis. Antigen can be own DNA in SLE.
Type 4: T cell mediated; CD4+ T cell activate APC cells, causing more damage than the virus
itself. CD4+ T cell activate macrophage. Cluster or APC become activated, called granuloma.
2. Unwanted immune reactions, auto-immunity:
Immunologic tolerance: why do we not attack our own proteins? Via central tolerance B
cells undergo deletion or receptor editing in the bone marrow. Peripheral tolerance an APC
presents a self-antigen, which when it is recognized by a T cell, it become anergic. Also, in
most times Treg suppress the B and T cells.
Auto immune diseases can occur via: genetic factors (diseases on MHC alleles) or via an
infection (co-stimulators or molecular mimicry):
- Co-stimulation: an APC presents a secondary stimulus, where the T cell reacts on
- Mimicry: via activation of microbe, recognize the wrong self-tissue.
SLE = auto immune disease where the antigen is a piece of DNA
Sjogren syndrome = auto-immune disease, causing destruction of the salivary glands.
Systemic sclerosis = auto-immune where too much extracellular matrix protein is made,
causing fibrosis (M2 macrophage) involving skin an parenchymal organs.
Transplant rejections:
Graft = the transplanted organ or tissue or cells
Recipient = the individual who receives the graft, also called the host
The adaptive immune system comes with its limitations. There are 3 typical immune
reactions with negative effects:
1. Hypersensitivity type I-IV
2. Unwanted immune reactions, like auto-immune or transplant rejections
3. Decreased immunity, due to immunodeficiencies.
Short recap immunology:
B lymphocytes become antibodies; Ig gene editing via 2 phases. Phase 1 is random, before
contact with the antigen happens in the bone marrow. Phase 2 is non random, occurs after
contact antigen to make it perfectly suitable, happens in the lymph nodes.
T lymphocytes become effector T cells. The CD4+ T cells bind antigen though their TCR that
is presented via MHC type 2. Become other t cells or memory t cells. Always an extracellular
antigen which is processed. The CD8+ T cell bind antigen via other TCR that is presented in
MHC type 1, always intracellular so mostly viruses.
1. Hypersensitivity
Type 1: allergy; upon activation of TH2 cells, IgE production starts. Binds to mast cells. Can
be an immediate hypersensitivity reaction (minutes) or late reaction (after repeated
exposure). Eosinophils are super active in allergy.
Type 2: antibody mediated; tissue damage or dysfunction due to antibodies binding to
receptors. Example is pemphigus vulgaris, antibodies against epidermal intercellular
adhesion molecule. Example is Graves’ disease, where the antibody bind to the TSH
receptor, constant thyrohyoid hormone secretion, hypermetabolic state. Example is
Myasthenia Gravis, antibody inhibits activation ACh recptor, less muscle activation.
Type 3: immune complex mediated; antigen-antibody complex, binding the vessel wall
causing further damage and induce phagocytosis. Antigen can be own DNA in SLE.
Type 4: T cell mediated; CD4+ T cell activate APC cells, causing more damage than the virus
itself. CD4+ T cell activate macrophage. Cluster or APC become activated, called granuloma.
2. Unwanted immune reactions, auto-immunity:
Immunologic tolerance: why do we not attack our own proteins? Via central tolerance B
cells undergo deletion or receptor editing in the bone marrow. Peripheral tolerance an APC
presents a self-antigen, which when it is recognized by a T cell, it become anergic. Also, in
most times Treg suppress the B and T cells.
Auto immune diseases can occur via: genetic factors (diseases on MHC alleles) or via an
infection (co-stimulators or molecular mimicry):
- Co-stimulation: an APC presents a secondary stimulus, where the T cell reacts on
- Mimicry: via activation of microbe, recognize the wrong self-tissue.
SLE = auto immune disease where the antigen is a piece of DNA
Sjogren syndrome = auto-immune disease, causing destruction of the salivary glands.
Systemic sclerosis = auto-immune where too much extracellular matrix protein is made,
causing fibrosis (M2 macrophage) involving skin an parenchymal organs.
Transplant rejections:
Graft = the transplanted organ or tissue or cells
Recipient = the individual who receives the graft, also called the host
