PCB 3233
PCB 3233 EXAM 5 STUDY GUIDE 2026
KNOW THE DIFFERENT CELLS THAT CAN BECOME PLASMA CELLS.
-activated B cells
-isotype switched, somatically hyper mutated centrocytes
-memory B cells
What are the components of the B cell co-receptor ( CR2 is one of them)
-CR2: complement receptor-2: binds to complement deposited on the pathogen
-CD19: receptor signaling
-CD81/TAPA-1: binds to CD19 and is essential and bringing it to the B cell surface
What does CR1 do for the co-receptor
CR1 binding to C3b on a pathogen facilitates the cleavage by factor I to ic3b and
C3d, then the CR2 component of the B cell co-receptor binds to C3d
What does TI antigen mean? What makes these different than TD antigens?
-TI stands for Thymus Independent . They activate production of Cells without T
lymphocyte involvement
-TD antigens are Thymus Dependents AGs. Bulk of pathogens specific AB are
produced by TD AGs. TD AGs are activate B cells in the secondary typhoid tissues.
Describe B cell activation, CD40 ligand, CD40, NFkB, ICAM-1 and IL-4 secretion by
T cells.
-Once B cells meet their antigen, the BCR and the co-receptor CXCL-13 calls B cells
to follicle. CCL-19/CCL-21 calls into the lymph nodes. These changes TRAP the B
cell in the Cell area close to the B cell zone. This allows for effector T-cells to test
their TCRs against the AG-MHC II on the B cell--> cognate interactions and
conjugate pairs.
-CD40 ligand expressed by T cells, to bind to CD40 on the B cell. Activates TF NFkB.
NFkB increases expression of adhesion molecule ICAM-1 to strengthen the
adhesion between the two cells.
-IL-4 is secreted by the T helper cells and allows for centrocyte differentiation into
memory B cells.
Define Follicular dendritic cells
PCB 3233
,PCB 3233
FDC are non-lymphoid cells of follicles in secondary lymphoid tissues. Their long
branching points make contact with B cells-they also have Fc and complement
receptors that hold Ag":Ab complexes on their surfaces. These cells are crucial in
selecting Ag-binding B cells during Ab response.
Define dark zones in follicular dendritic cells
In the dark zones, there are closely packed centroblasts and FDCs secrete those
below for proliferation:
1. IL-6
2. IL-15
3. 8D6
4. BAFF
Define light zones in follicular dendritic cells
In the light zones, slowly to non-dividing centrocytes will interact with antigens
held by FDC's
what is in each of the zones?
-Dark zone: there are FDCs which secrete IL-6, IL-5, 8D6, and BAFF to proliferate.
-close packed proliferating centroblasts and T cells
-T follicular helper cells attached to B -cells interacting with CD40 induce B cells to
make AID --> somatic hypermutation and biotype switching
What happens to the cells in the zones?
-Centrocytes move from GC dark zone-->capture antigen from FDC--> moves to GC
light zone outer regions to helper T cells
-In dark zones:
1. 80% centroblasts
2. Rapidly dividing activated B cells
3. Going through somatic hypermutation and isotope switching
4. No BCR on surface
5. B cells secrete AID
-In light zone: 10-20% centrocytes
a. slowly non-dividing B cells with mutated , isotope switched BCR
b. express BCR again to test against antigen
PCB 3233
, PCB 3233
How do antibodies function? Do they destroy the pathogen directly or do they tag
and cover up things?
a. antibodies aim to neutralize the pathogen (doesn't destroy)
b. activates complement via classical pathway
c.opsonization- tagging pathogens for phagocytosis
What is the B cells role in its activation? And what are the steps in B cell activation
in the lymph node. (Know steps)
a. Antigen binding (does the B cell take up the antigen, what is this called)
i. Antigen binding (does the B cell take up the antigen, what is this called) TD
antigen: BCR signal + B cell coreceptor signal + TH2 signals (CD40:CD40L and
cytokines); B cell takes up TD antigen by receptor mediated endocytosis.
ii. TI-1 antigen: BCR signal + b cell coreceptor signal + antigen bound to additional
surface receptor
iii. TI-2 antigen: BCR signal + B cell coreceptor signal + extensive cross-linking
caused by repetitive epitopes on pathogen surface; results in early Ab response;
limited, no isotype switching, no hypermutation, no long-term memory.
iv. Binding of Ag sends a signal to the B cells nucleus to change gene expression.
Yep, the B cells take up the antigen by internalizing Ag by receptor mediated
endocytosis which processes and presents it to Th cells.
b. What are cognate interactions
i. Cognate interactions are cell-cell interactions between B and T lymphocytes
specific for the same antigen. Occurs when Antigen Activated B cells present
antigen to a Thelper cell.
c. Primary focus? Where is this and what is the major isotype made here.
i. Temporary aggregate of proliferating activated Ag-specific B cells and T cells that
form in the secondary lymphoid tissue at the beginning of the adaptive immune
response. Forms when mature, naïve B cell is activated by a TH2 cell. Primary
focus will develop into a germinal center within a week
ii. Occurs in the medullary cords.
iii. Major isotype made is IgM.
d. Medullary cords
i. Found near the efferent lymphatic vessels where some of the b lymphoblasts
stay to differentiate into plasma cells under influence of IL-5 and IL-6
PCB 3233
PCB 3233 EXAM 5 STUDY GUIDE 2026
KNOW THE DIFFERENT CELLS THAT CAN BECOME PLASMA CELLS.
-activated B cells
-isotype switched, somatically hyper mutated centrocytes
-memory B cells
What are the components of the B cell co-receptor ( CR2 is one of them)
-CR2: complement receptor-2: binds to complement deposited on the pathogen
-CD19: receptor signaling
-CD81/TAPA-1: binds to CD19 and is essential and bringing it to the B cell surface
What does CR1 do for the co-receptor
CR1 binding to C3b on a pathogen facilitates the cleavage by factor I to ic3b and
C3d, then the CR2 component of the B cell co-receptor binds to C3d
What does TI antigen mean? What makes these different than TD antigens?
-TI stands for Thymus Independent . They activate production of Cells without T
lymphocyte involvement
-TD antigens are Thymus Dependents AGs. Bulk of pathogens specific AB are
produced by TD AGs. TD AGs are activate B cells in the secondary typhoid tissues.
Describe B cell activation, CD40 ligand, CD40, NFkB, ICAM-1 and IL-4 secretion by
T cells.
-Once B cells meet their antigen, the BCR and the co-receptor CXCL-13 calls B cells
to follicle. CCL-19/CCL-21 calls into the lymph nodes. These changes TRAP the B
cell in the Cell area close to the B cell zone. This allows for effector T-cells to test
their TCRs against the AG-MHC II on the B cell--> cognate interactions and
conjugate pairs.
-CD40 ligand expressed by T cells, to bind to CD40 on the B cell. Activates TF NFkB.
NFkB increases expression of adhesion molecule ICAM-1 to strengthen the
adhesion between the two cells.
-IL-4 is secreted by the T helper cells and allows for centrocyte differentiation into
memory B cells.
Define Follicular dendritic cells
PCB 3233
,PCB 3233
FDC are non-lymphoid cells of follicles in secondary lymphoid tissues. Their long
branching points make contact with B cells-they also have Fc and complement
receptors that hold Ag":Ab complexes on their surfaces. These cells are crucial in
selecting Ag-binding B cells during Ab response.
Define dark zones in follicular dendritic cells
In the dark zones, there are closely packed centroblasts and FDCs secrete those
below for proliferation:
1. IL-6
2. IL-15
3. 8D6
4. BAFF
Define light zones in follicular dendritic cells
In the light zones, slowly to non-dividing centrocytes will interact with antigens
held by FDC's
what is in each of the zones?
-Dark zone: there are FDCs which secrete IL-6, IL-5, 8D6, and BAFF to proliferate.
-close packed proliferating centroblasts and T cells
-T follicular helper cells attached to B -cells interacting with CD40 induce B cells to
make AID --> somatic hypermutation and biotype switching
What happens to the cells in the zones?
-Centrocytes move from GC dark zone-->capture antigen from FDC--> moves to GC
light zone outer regions to helper T cells
-In dark zones:
1. 80% centroblasts
2. Rapidly dividing activated B cells
3. Going through somatic hypermutation and isotope switching
4. No BCR on surface
5. B cells secrete AID
-In light zone: 10-20% centrocytes
a. slowly non-dividing B cells with mutated , isotope switched BCR
b. express BCR again to test against antigen
PCB 3233
, PCB 3233
How do antibodies function? Do they destroy the pathogen directly or do they tag
and cover up things?
a. antibodies aim to neutralize the pathogen (doesn't destroy)
b. activates complement via classical pathway
c.opsonization- tagging pathogens for phagocytosis
What is the B cells role in its activation? And what are the steps in B cell activation
in the lymph node. (Know steps)
a. Antigen binding (does the B cell take up the antigen, what is this called)
i. Antigen binding (does the B cell take up the antigen, what is this called) TD
antigen: BCR signal + B cell coreceptor signal + TH2 signals (CD40:CD40L and
cytokines); B cell takes up TD antigen by receptor mediated endocytosis.
ii. TI-1 antigen: BCR signal + b cell coreceptor signal + antigen bound to additional
surface receptor
iii. TI-2 antigen: BCR signal + B cell coreceptor signal + extensive cross-linking
caused by repetitive epitopes on pathogen surface; results in early Ab response;
limited, no isotype switching, no hypermutation, no long-term memory.
iv. Binding of Ag sends a signal to the B cells nucleus to change gene expression.
Yep, the B cells take up the antigen by internalizing Ag by receptor mediated
endocytosis which processes and presents it to Th cells.
b. What are cognate interactions
i. Cognate interactions are cell-cell interactions between B and T lymphocytes
specific for the same antigen. Occurs when Antigen Activated B cells present
antigen to a Thelper cell.
c. Primary focus? Where is this and what is the major isotype made here.
i. Temporary aggregate of proliferating activated Ag-specific B cells and T cells that
form in the secondary lymphoid tissue at the beginning of the adaptive immune
response. Forms when mature, naïve B cell is activated by a TH2 cell. Primary
focus will develop into a germinal center within a week
ii. Occurs in the medullary cords.
iii. Major isotype made is IgM.
d. Medullary cords
i. Found near the efferent lymphatic vessels where some of the b lymphoblasts
stay to differentiate into plasma cells under influence of IL-5 and IL-6
PCB 3233
