Exam 1 9/28 Kingsley Immuno Flashcards
BCR recognizes ____ antigen
soluble
What proteins/components are involved with BCR Signal 1?
CD79 a/b or Ig-alpha and Ig-beta
What proteins/components are involved with BCR Signal 2?
CD21 recognizes C3d (breakdown of complement 3)
What is CD21?
complement receptor on B cell membrane
What is presented to T cells?
antigen-antibody complex via MHC I or II
Which cells are considered antigen presenting cells?
macrophages, B cells
A foreign antigen is presented to T cell (TCR) as:
non-self
True or false: TCR on T cells can recognize soluble antigens
False - this is for B cells
TCR recognizes only complexed/bound antigen by MHC
What protein is involved with signal transduction in TCR?
CD3
Which MHC does CD4 T-helper cells recognize?
MHC II
This is for exogenous or “found” antigens
Th1 is involved with what APC?
macrophages –> mainly involved with inflammation
Th2 is involved with what APC?
B-lymphocytes –> mainly involved with humoral response
Clonal expansion
Clonal selection –> that B cell starts to divide rapidly and differentiate into plasma cells which secrete antibody
- memory B cells retain BCR
Clonal expansion allows for what kind of response?
2ndary anamnestic
T-dependent responses
- most antigens, usually complex proteins
- multiple, different determinants
- efficient response, memory –> B memory cells formed
T-independent responses
- polysaccharides, LPS, nucleic acids
- repeated determinants, usually IgM response
- weak, no memory
Immunologic memory definition
B and T cells following activation; larger number of existing cellls with specific receptor for particular antigen
One activated B cell can produce up to how many plasma cells?
4000
B cell surface Ig - high or low?
High
Plasma cell surface Ig - high or low?
Low
Does B cell have surface MHC II?
Yes
Does plasma cell have surface MHC II?
No
Do B cells secrete Ig?
No
Do plasma cells secrete Ig?
Yes
Is there growth in B cells?
Yes
Is there growth in plasma cells?
No
Can B cells undergo isotype (class) switching?
Yes
Can plasma cells undergo isotype (class) switching?
No
Primary antibody produced
IgM
Primary antibody production lag time
7-10 days
Secondary response activates:
memory B cells (have IgM); rapid shift to produce IgG
Secondary response lag time
1-4 days
Affinity maturation
- IgG is formed due to class switching after secondary response, has higher affinity for antigen than IgM
- highest affinity B cells selected by binding to antigen on follicular dendritic cells
Lag phase
time between antigen exposure and antibody response
Which part of the antibody changes during class switching?
Only the CH. VH and light chain do not change
When class switching occurs, what is preserved?
The idiotype (antigen combining site)
What is the directionality of class switching?
Unidirectional (ex: IgE can’t go to IgM, IgG, or IgA)
IgG class switching requirements
IL-4 and IFN-gamma
IgA class switching requirements
IL-4 and TGF-B
IgE class switching
IL-4 by itself
Memory B cells are activated (faster/slower) than naive B cells, leading to:
faster; shorter lag phase
Where are memory IgA cells/plasma cells formed?
Near mucosae
Where do B and T cells get activated?
- external facing mucus-lined surfaces (MALT, GALT)
- lymphatic drainage sites (lymph nodes)
Where are B cells found in lymph nodes?
cluster (follicle) cortex
Where are T-cells found in lymph nodes?
Paracortex/parafollicular cortex (either name)
What happens in the lymph node when antigen enters afferent lymph vessel?
Germinal center develops; B and T cells found in secondary follicle
Waldeyer’s ring is composed of:
- pharyngeal tonsil/adenoid
- 2 tubal tonsils
- 2 palatine tonsils
- lingual tonsil
What is the function of the germinal center?
Active site of B cell proliferation and differentiation within secondary follicles
B cell doubling time
6 hours
True or false: class switching occurs in germinal center
True
Antibody molecules include a ____ ____ set of antigen-binding sequences
potentially unlimited
Somatic hyper mutation and recombination is also known as:
variable domain recombination (DNA rearrangement) - somatic recombination of VDJ DNA
What areas of the body does somatic recombination occur?
Bone marrow and thymus
Where does somatic recombination occur?
Hypervariable regions of BCR and TCR
X-linked severe combined immunodeficiency (XL-SCID) - what is the cause?
IL-2 receptor has reduced function; required for B and T cell development and proliferation (in the chart, says there is much less T cells)
Leads to non-functional IL-7 function in the thymus
Who is more likely to be affected by XL-SCID?
Males - since it is X-linked
What is the cause of DiGeorge syndrome?
22q11.2 deletion syndrome; thymic aplasia
DiGeorge syndrome is mainly acquired via:
de novo deletion
Main symptoms/clinical manifestations of DiGeorge syndrome
Cleft palate, other craniofacial disorders
What gene is affected in DiGeorge syndrome?
TBX1 - responsible for pharyngeal pouches
“complete” depletion of TBX1 results in:
Absence of thymus in DiGeorge syndrome
Pharyngeal pouch 3
Thymus
Pharyngeal pouch 4
Superior parathyroid gland
Bare lymphocyte syndrome 1 (BLS1) is known as:
MHC1 deficiency
Bare lymphocyte syndrome 1 (BLS1) is caused by:
Mutations in TAP1 - does not allow normal protein complex with MHC1
Bare lymphocyte syndrome 2 (BLS2) is known as:
MHC II deficiency - does not allow foreign antigens to complex with MHC II
MHC deficiency means that you cannot:
Class switch/clonal expansion
What happens to CD8/CTL in BLS1?
not able to detect pathogens; leads to intracellular parasites and viral infection
BLS II is a form of:
SCID –> TH1 and TH2 responses are non-functional
Heterotaxy syndrome
Internal thoracic-abdominal organs exhibit abnormal arrangements across left-right axis
Asplenia heterotaxy syndrome
Missing spleen entirely
Spleen is a major site for:
Antibody production
Polysplenia heterotaxy syndrome
Multiple small accessory spleens with reduced function; other organs like thymus may be affected
What disease do you see a 350-fold increased risk of bacterial sepsis?
Isolated congenital asplenia
What bacteria are commonly found to cause infection in isolated congenital asplenia?
Polysaccharide encapsulated bacteria
Pemphigus antibody/targeted structure
Auto-antibodies IgG against desmoglein-3 of desmosome
Pemphigoid targeted structure
autoantibodies to BP-1 of BMZ, hemidesmosome
Linear IgA targeted structure
Linear IgA deposition in BMZ
EBA autoantibody/targeted structure
Auto-immunity IgG develops against Type VII procollagen
Pemphigoid is characterized as:
cicatricial (mucous membrane) - oral
Goodpasture syndrome
Autoantibodies to alpha-3 subunit of Type IV collagen
