Protein Function Pathway

CD34 On all Hemopoetic Stem cells

CD21 (CR2) -iC3b + C3d co-receptor Involved in Complement
Connects the B cell to the cascade and B cell activation
complement cascade
-CR2+ C3d allows intercellular
stimulation which is an increase
in overall signaling
CD19 Signaling chain of co- Involved in B cell marking
receptor/B-cell marker
CD 81 BCR/ Co-receptor interaction Entry point for HCV (hep C)
CR1 Recognizer of C3b
CCL 21/19 Cytokines that attract cells to B cell activation
the LN, ones with CCR 7 T cell activation
Immature DC cells without
antigens
CXCL 13 Allows B-cells to enter, B-cells
follow a gradient of CXCL-13
CD 69 Expressed after Antigen B cell activation
encounter on B-cells blocks
S1P
S1P A chemotactic lipid that binds to
a receptor on Naive T-cell.
Blocked by CD69.**** [verify]
IL-5 Involved in Plasma cell
formation [derived from B cell]
Produced from Th2
IL-6 -Secreted by T-cells to induce
plasma formation
-FDC’s secrete this in
centroblast formation
-In combination with IL-1 and
TNF-α, it leads to a high
inflammatory response
IL-15 FDC’s secrete this in centroblast
formation
Involved in the proliferation and
growth of NK cells as well
[book]
BAFF FDC’s secrete this in centroblast
formation
BCL-xL Survival signal originating from
the ligation of MH-II and CD40
on B cell and T-cell combination
IL-10 Used in the differentiation of
plasma cells in centrocytes
Produced by T-regulatory Cells
IL-4 Used in Centrocyte
differentiation into memory B-
cells Produced from Th2
FcRn It is involved in the movement
of IgG from the blood stream to
the inside of the tissue.
It binds the Ab within the cell
and protects from the lysosome
by the binding to the Fc Region
pIg Is involved in the transport of
IgA across membrane
It is cleaved during this process
and keeps a piece of itself
attached to the A
FcεR1 Allows for the readily binding of
IgE to allow an allergic reaction
Found on: neutrophils, Mast
cells, Eosinophils
CRP Involved in the binding of IgM

FcγR Binds IgG

CD16 Binds to FcγRIII on NK cells and
tells it to kill
FcγRIII Binds CD16, found on NK cells
RAG Recombination protein gene
necessary for the formation of
different classes of Ig’s.
-Issues found with this gene
leads to a deficiency in Ig
Production
-Mechanism is a Dimer
formation for initiation of
recombination
RSS One/both ends of VDJ
recognition by the RAG-1 and
RAG-2
-It follows this recognition by
direction of recombination,
ensuring that correct processes
occur
CD3 Complex CD3ε(2) + CD38+CD3γ+ζ
IL-7 Required for further B-cell
growth and proliferation with
receptors found on both late
pro and pre-B cell
-Cytokine necessary in T-Cell
development produced by
thymic stroma and bind to the
CD34 expressing progenitor
cells
pTα β chain test for ability for ability
to bind to its Ag (β – won at this
point
L-Selectin T-cell binder to to sialyl-lewisx of
CD34 and GlyCAM-1
CD34 Used to carry T cells in rolling
mechanism
GlyCAM-1 Found on HEV, used to carry the
T-cell to its destination
ICAM1 and ICAM2 Binds to LFA to stop movement
when the T-cell arrives to the LN
DC cell binding T-Cell - DC cell
CD2 LFA3
LFA-1 ICAM 1 / 2
ICAM 3 DC SIGN
TNF-α Massive increase in production
leads to septic shock

IL-1+TNF-α are key to an

inflammatory response

IL-1β Fibroblast interferon production

that is key in viral infection
resistance
Increases inflammation
IL-1 In concert with TNF-, it plays a
key to an inflammatory
response
IL-12 Macrophage cytokine that acts
on NK cells
Produced by Th1
Dectin -1 Phagocytosis macrophage
receptor that recognizes
carbohydrate ligands
Mannose receptor Dendritic cell[non-follicular] and
macrophage receptor that
pushes for pathogen
phagocytosis
MARCO Scavenger receptor on
macrophage that binds to both
gram negative and positive
Selectin Required by neutrophils to
enter into inflammatory
response
NLR’s Coreceptors, Nod-1 and Nod 2
Its function is to detect the
products derived from
 intracellular degraded
phagocytosed pathogens
B7 A B-cell Receptor that binds to
CD28 on a T-cell that allows
further growth
IL-2 Get produced in in an autocrine
way, acts on IL-2R for higher
proliferation
Cyclosporine A, FK506 Inhibits IL-2
Rapamycin IL-2 Receptor inhibition
TH1+TH7 In patients with a lack of IL-10
receptor, patients produce this
combo to be mediated on
subsets of CD4-T cells
CD4 Tfh They remain in the secondary
lymph node and proliferate B-
cells with the receptors of CD28
–B7 and CD40L
VLA-4 Replaces CD62C on L-selelctin
and binds to VCAM-1 On T-Cell
for the purpose of homing into
the inflamed tissue.
CD2+LFA-1 Effector T cells use this to
become more sensitive to tissue
than Niave T-cells
Th1 Cells produces IFNγ and IL-12 (in a
positive feedback loop) in a
feedback loop for pro immune
responses to in order for
macrophages to suppress
intracellular infections
IFNγ -Produced by Th1 cells to
stimulate immune response
Will stimulate macrophages and
remain in the synapses.
-Combined with MHCII it
induces transcription of class II
cells
-Combined with protostomes it
causes a high production of
proteasomes in LMPC, as well
as an increase in p28 release
-Combined with DO under
states of noninfection, DM in
states of infection
-combination of CD40 leads to
increased expression of IL-12 on
 DC cells which leads to more NK
T cells
Th17 Produces IL-17,21,22,26 to
enhance the neutrophil
response to fungal and
extracellular bacterial infections
It is induced by IL-6 and TGF-β
Th2: Antagonist to Th1(anti-
inflammatory)
Helps in allergic reactions with
mast cells, eosinophils,
basophils, and B cell IgE
responses

Induced by IL-4
Produces IL-4 and IL-5

TfH Helps B cells differentiate and

class switch
It is induced by IL-16, TGF-β,and
IL-23
T regulatory cells Down Regulates T-cell Function
Induces by: TGF-β
Produces TGF-β and IL-10
JAKs Non-binding cytokine receptors
that Allow Stats to bind upon
phosphorylation
And activates transcription
STATS Activate transcription upon JAK
phosphorylation
SOC’s Bind tyrosine on the cytokine
receptor
Th2 secretion TGF-β + IL4+IL-10 +IL-13
CD25 Expressed on T-regulatory cells
in order to suppress T-cells
FOXD3- It is a transcription suppressor
produced by T-regulatory cells
Perorin+granulysin+serlycin Hole formation in the cell
Grazymes Degenerate nucleus and cause
shrinkage by CD8
NKg2D Expressed by NK cells upon
activation.
Activates MHC-Like structures
It is found in high quantities
during stress
CD16a[FCγRIIIA] Receptor found on NK cells
 Only receptor needed for
activation during adaptive
immunity
IgG specific
CD94: NKG2A Ligated by HLA-E [Corralated
with HLA- [A-C]
MIC glycoproteins Activated during stressed
allowing NKG2D to bind
KIR Inhibitory receptor that
recognizes diff forms of HLA
receptors
CD94: NKG2C Predominant during CMV
infection, high cytotoxic activity,
and low responsiveness to
cytokines
Type matching MHC complexes HLA: A,B, and DR
required:
HLA-[A,B,C] Highly polymorphic, Ag to CD8
NK ligands
MHI
MHCII DP, DQ, DR
AG to CD4 T-cell
DM +DO Oligimorphic regulate peptide
FCyRI Receptor of IgC3
Pentaxins Access of protein in the blood
that targets pathogens for
destruction
C-reactive proteins
CD-14 Co-receptors to TLR4, its making
macrophage
CXCL8 Macrophages secrete it upon
activation to attract necessary
cells to migrate from blood to
tissue
IL-1β
Calnexin Stabilizes MHC1 after synthesis
to prevent mis-folding of till the
attachment of β2 microglobin
Taposin Stabilizes MHC to receive
peptides
ERAP Acts like pacman to shorten
long peptides bound to MHC1
till its ready to present itself
iI It is th einvariant chain and
blocks MHCII from binding to
class I peptides
CLIP Broken down iI that remains
attached to MHC2 till it binds to
till HLA-DM binds
HLA-DM Similar to MHC2 and acts to free
up CLIP from MHC2
Remains bound till MH2 bound
to right antigen
HLA-DO Reversibly binds to MHC2 to
inhibit Ag presentation
CCR7 “seeker protein” receptor on
B/T cell that seeks out gradients
of CCL 21 and 19
CCL 21/19 Released by DC’s to attract T
and B cells
IPP Stress molecule that at normal
physiological levels illicit no
response
HMBPP Stronger than IPP made by
bacteria and parasites
BHPP Bind with FCrs at the same time
to induce a T-like cell Vγ:Vδ to
perform ADCC and kill B cell
lymphoma
Zolendronate High Ipp, allows therapeutic
function to fix bone
BTN3A1 Found on all sells, and is
structurally similar to B7,
allowing T like cells to bind.
Specific cobinding from Vγ9:Vδ2
Vγ9:Vδ2 Recognizes phosphoten and not
peptides, binds using BTN3A1
EPCR Ligand for Vγ4:Vδ5 similar to
MH! And allows its cell ti bind
directly
CD1D Group 2 of the CD1 and binds to
Vγ:Vδ
Vγ:Vδ Binds long hydrophibic alkyl
chains.
Ag presented by CD1d
α:β T cells that are non polymorphic
MHC1
Bind CD1a, b, c
NKT cells Bind CD1d
MAIT cells Small organic molecules on MR1
is how it recognizes stuff
CD8 like,
Il12R Activated by IL-18, 23, 25
IgG4 High affinity for all IgG’s
It stimulates FcRIIβ
FCγRIIB Activates macrophages and
neutrophils by antibodies
IGE Most likely picked up by mast
cells on the FcεRI
FcεRII 2 receptor for IgE on mast cells
Each binding domain will bind
single IgG molecule
Can directly bind to IgE, BCR,
BCR co receptor, CR2
ADAM-10 cleaves FcεRII at different sigts
Produces monomeric/ Trimeric
FcεRII
Prostaglandins Promotes BV diliation
Chemoattractors for PMNs
Mast Cells Will synthesize IL-4, TNFα
Eosinophils CCL5. CCL7, CCL11, CCL13
CD27 Marker on B cell
FCγRIIBI Niave B cells suppressor
(Ag+Ab)