Immunopathology Flashcards
how does a normal immune response cause disease
damage from inflammation in response to pathogen can exceed the damage done by the pathogen
three infections that trigger a damaging immune response
- tuberculosis
- leprosy
- sarcoidosis
hypersensitivity
altered immune response to an antigen which results in disease or damage
allergy (atopy)
hypersensitvity to environmental allergies
autoimmunity
hyper sensitivity to self-antigens
alloimmunity
reaction to antigens from someone else
four types of hypersensitivity
Type 1: IgE mediated (anaphylaxis)
Type 2: cytotoxic reaction to self allergens (lmyastheia gravis)
Type 3: immune complex reactions (lupus)
Type 4: cell mediated (chronic transplant reaction)
what is the difference between atopic individuals and non atopic
atopic individuals developed more Th1 lymphocytes vs Th2
how does IgE cause atopy
IgE binds to mast cells, which degranulate and release high amounts of histamine
where are three locations of concentrated mast cells
- skin
- airway mucosa
- GI
what is the physical interaction between allergens and IgE on mast cell receptors
IgE binds to mast cells, allergens form cross links between IgE to produce a stronger response
what is the difference between Th1 and Th2
helper lymphocyte 1 produces more IgG
Th2 produces more IgE
why do some people produce more Th2 lymphcytes
the mechanism isn;t know but may be related to the hygiene hypothesis
what is the potential link between infection and allergies
exposure to bacterial infection increases the production of Th1, if there is no infection exposure then Th2 dominates
what is the cut off age that a person must be exposed to certain antigens to produce more Th1 cells vs Th2 cells
exposure before age 2 will result in more Th1 cells, after more Th2 cells
T/F everyone has the potential for autoimmune disease
True, everyone has some defective cells
genetic risk factors for autoimmune disorders
family and species genetics
civilization hypothesis
the formation of cities with close proximity of people and animals increased the number of epidemics and pandemics
this created an evolutionary pressure to develop a strong resistance to infection but decreased our ability to regulate immune response to self antigens and neoplasm
autoimmune pathophysiology
T cell antigen receptors will bind with antigens they have a lower affinity for (like self antigens) if they are activated molecular mimicry
molecular mimicry
when an autoimmune disease is triggered by an infection due to T cell cross reactivity
two examples of molecular mimicry
- strep pyogenes and rheumatic fever
- coxsackie and type I diabetes
antigen spreadng
what specific disease can this cause
when damage from an intial autoimmune response allows T and B cells to cross react with other self antigens
can cause lupus
what are four ways to treat autoimmune disease
- decrease number of lymphocytes
- reduce production of antibodies
- interfere with T cell activation
- reduce cytokines (interleukin and tumor necrosis factor)
two categories of immunodeficiency symdromes
- congenital
- acquired
three examples of congenital immunodeficiency
- isolated T cell deficiency
- isolated B cell deficiency
- SCIDS
what lymphocyte does HIV attack to cause AIDs
CD4 helper T cells
what are four causes of acquired immunodeficiency
- AIDS
- immunosuppressive therapy
- inadequate nutrition
- tuberculosis
what are the symptoms of acute HIV infection
flu like symptoms that occur 2-4 weeks after exposure and last 1-4 weeks
latent HIV infection
gradually decreasing CD4 counts and increasing viral load
what are three factors that influence the length of the latent phase of AIDS
- nutrition
- other diseases
- antiviral treatment
what is the goal of current HIV treatment
prolonging the latent phase
what is the primary indicator of the AIDS phase of an HIV infection
opportunisitc infection or unusualy cancer
if an HIV positive patient is diagnosed with leukemia and receives a blood marrow transplant which decreases the amount of HIV in his blood, what happened
the bone marrow donation was homozygous for a chemokine receptor mutation which removed the receptor needed for HIV to bind with CD4 cells
why is there a difference between HIV mortality in developed countries vs Africa
because developed nations have better nutrition, less exposure to disease, and better access to healthcare
what is an example of an excessive immune response
cytokine storm
what causes cytokine storm
introduction of super antigens that cause a feedback loop leading to excessive activation of cytokines and their effectors
what are two historical instances of cytokine storm
- 1918 flu pandemic
- 2006 trail of CD28 agonist monoclonal antibodies
why was the flu of 1918 unique?
how did most people die?
it was most fatal in young healthy people due to cytokine storm
either from intial cytokine storm or secondary pneumonia
how is cytokine storm relevant to modern cancer therapy
what is the risk of this therapy?
patient T cells can be modified in vitro and given back to the patient to target cancer cells
it can cause a cytokine storm
what are two sources of “super antigens”?
what are two pathologies associated with cytokine release
bacterial toxins or viral proteins
toxic shock and septic shock
