Download Q:1:- The physiologic functions of Immune Reactions? Ans

Q:1:- The physiologic functions of Immune Reactions?
Ans:- Functions of Immune reactions:- 1)-Immunological defense. -Prevention of pathogens
-Removing the invaded pathogens 2)-Immunological surveillance -Removing mutant cellsRemoving injured or decrepit cells 3)-Immunological homeostasis -Immune regulation
-immune tolerance
Q:2:- Composition of Immune system?
Ans:- a complex system consists of -1.immune organs & tissues,
-2.immune cells,3. immune
molecules, responsible for immunity.
Q:3:- Types of Immune responses?
Ans:- Immune response:- a coordinated response against the foreign substances.
Two Types:1)-Innate immune response, (Non-specific immunity):- e.g:- the cell, the
molecule. 2)- Adaptive immune response, (specific immunity):- e.g:- T-lymphocyte, Blymphocyte, Antibodies, Effector T cells.
Q:4:-Lymphocyte homing?
Ans:- Lymphocyte Homing: The process that mature lymphocytes leave primary lymphoid
organ through blood, reside in the particular sites of secondary lymphoid organs.
Q:5:-Lymphocyte Recirculation?
Ans:- Lymphocyte Recirculation: Continuous movement of lymphocytes through blood, lymph,
lymphoid organs, and tissues.
Q:6:-BM & Thymus?
Ans:- Bone Marrow(BM): (1)Development of blood cells.-All the immune cells -Pro-T
(2)Generation & maturation of B cells.(3)The site of B cell-mediated immune responses:-Plasma→back to BM→antibody. Thymus: (1)T cells development & maturate (to be the sites
where T cells reach a stage of functional maturity). (2)Set up immunological tolerance of T cells.
(3)Immune regulation.
Q:7:-Lymph Node, Spleen, & Malt?
Ans:-Lymph node: (1) The major site for mature B and T cells residing. (2) The site where T &
B cells response to Ag. (3) Take part in lymphocyte recirculation.(4) The organs filtrating and
cleaning the Ag from tissue. Spleen: (1) The major site for mature B and T cells residing
(2) The site where T & B cells response to Ag. (3) The organs filtrating and cleaning the Ags
from blood. Malt:The tissues where T & B cells response to Ag from mucosa.The tissues
generating sIgA. The site for mature B and T cells residing.
Q:8:-Heterohpilic Ag?
Ans:-A kind of common epitope Ags that present between the individuals of various species.
Q:9:- Idiotypic Ag?
Ans:- A kind of self Ag that is present in the Ag binding site of an Ag receptor in an
individual.
Q:10:- Superantigen?
Ans:- An Ag that activates different T cell clones by directly binding to both TCR and MHC
molecule of APC from outside.
Q:11:- Comparison b/w T & B epitopes?
T epitope
Receptor
MHC
Property
Epitope
Position
TCR
Necessary
Denatured
Saquential
At any part
B cell: recognize intact Ag
,,
B epitope
AB / BCR
Not need
Native
Sequential or conformational
On the surface
T cell: recognize processed Ag
Q:12:- Monoclonal Ab?
Ans:- An antibody produced by a clone or genetically homogenous fast-growing cell i.e.,
hybridoma. They are widely used in cancer detection, diagnosis, and treatment.
Q:13:- Genetic engineering Ab?
Ans:- The Abs expressed by recombined Ig gene that was deleted, spliced or revised before
transferred into cells.
Q:14:- Function of Ig?
Ans:- (1) Neutralization:CDR/HVR (in V region) bind to: Microbial surface molecules to
inhibit the microbe to interact with cellular receptor of host. -Microbial toxins to inhibit the
interaction between toxins and cellular receptor of host.(2) Opsonization: (Ab-Mediated
Opsonization) -CDR/HVR of Ab specifically bind to Ag of microbe.. -Fc of Ab(IgG) bind to FcR
on Phagocytes (Mf/Neutrophil). -The Abs enhance phagocytosis efficiently and specifically.
(3)Complement activation: Classical Pathway of Complement activation is activated by the Ab
(IgG/IgM) that specifically bind to Ag.(4)Mediation od ADCC : (Ab-Dependent Cell-Mediated
Cytotoxicity) -CDR/HVR of Ab specifically bind to Ag of target cell (virus infected cell).
-Fc of Ab(IgG) bind to FcR on NK cell.
-The Abs enhance NK to kill the target cell .
Q:15:- Characteristics of IgA?
Ans:-SIgA Mediates Mucosal Immune
-Colostrum (neonate). -External secretion; alimentary
tract ,respiratory tract ,lacteal gland ,salivary gland ,tear gland.
Q:16:- Characteristics of IgD?
Ans:-1) mIg (BCR). 2)Marker of mature B cell.
Q:17:- Characteristics of IgE?
Ans:-Mediate type I Hypersensitivity.
Q:18:- Characteristica of IgG?
Ans:-1)Most rich in blood. 2)Longest half life. 3)Major Ab in 2nd immune response.
4)Highest Affinity. 5)Pass placenta.
Q:19:- Characteristics of IgM?
Ans:-1)Produced earliest in immune responses;-1st line defense against infection.
-Early diagnosis of infection.2)Produced earliest in ontogenesis;-diagnosis of intra-uterine
infection (Cord Blood).3)Pentamer is strong in; -Ag binding ability.-Complement activation.
Q:20:- Complement?
Ans:-A group of serum and cell surface proteins
that acquire activity by sequential
activation. They exhibit multiple effects in immune responses.
Q:21:- Functions of Complement System?
Ans:- 1.Cell lysis.2.Opsonization.3.Inflammatory Mediator.4.Immune Adhesion.
Q:22:- Cytokines (CK)?
Ans:-Cytokines are polypeptides produced in response to antigens and they effect as regulators
of intercellular communication in immune responses.
Q:23:- Secretary features of CKs (cytokines)?
Ans:- 1)autocrine, 2)paracrine, 3)endocrine.
Q:24:- Effect features of CKs (cytokines)?
Ans:-1)pleiotropism, 2)redundancy, 3)synergy, 4)antagonism.
Q:25:- Functions of CKs (cytokines)?
Ans:-1.Innate immune regulation.2.Adaptive immune regulation.3.Stimulating hemopoiesis.
4.Target cell killing.5.Promoting repair in trauma.
Q:26:- CAM (cell adhesion molecule)?
Ans:-The Molecules mediating contact and binding between cell
and cell or between cells and
extracellular matrix.
Q:27:- LDA (leukocyte differentiation antigen)?
Ans:-The surface molecules that appear on or disappear from cell membrane during cell
differentiation, development, activation.
Q:28:- Functions of CAM ( cell adhesion molecule)?
Ans:-1. Co-receptors & accessory molecules.2. Interaction of leukocytes with vascular
endothelium in inflammation. 3. Lymphocyte homing.
Q:29:- Concept of MHC?
Ans:-MHC is a large gene complex located on a single chromosome, which encode molecules
involve in vigorous rejection of grafts and antigen presentation.MHC present in all mammalian
species.-MHC in human is called HLA (Human Leukocyte Antigen)-MHC in mouse is called H2.
Q:30:- Functions of Classical MHC-I, MHC-II Molecules?
Ans:-1. Present Ag for T cells to initiate T cell immune responses. 2.When T cells recognize Ag,
mediate MHC restriction. 3.During thymocytes developing, mediate T cell selection.
Q:31:-V(D)J Recombination?
Ans:-1. Antigen receptor genes consist with many V,D, and J gene segments next to RSS.
2. Recombinase RAG1/RAG2 recognize RSS and cooperate with other enzymes to mediate
rearrangement of V(D)J segments.RESULT: multiple V, D, and J gene segments may combine
randomly, so as to generate a great number of combinations of Ig V region.
Q:32:-V(D)J Junction?
Ans:-During V(D)J recombination, one to several nucleotides
can be added to or removed
from the DNA end generated by RAGs, which increase antigen receptor diversity greatly.
Q:33:-Somatic Hypermutation?
Ans:-In proliferating germinal center B cells that finished V(D)J recombination, the Ig V
genes undergo point mutation at a very high rate, which plays a very important role in affinity
maturation.
Q:34:-B Cell Clonal Deletion?
Ans:-In bone marrow, immature B cells binding self-Ag with mIgM can cause die by apoptosis,
so as to remove the self-reactive B cell clones.
Q:35:-Features of B1 & B2 cells?
FEATURES
Specificity
Renew
TH assist
Memory B
Major Ig class
Ag
Origin time
Distribution
B=1
B=2
Poor
Self
(=)
(=)
IgM
Carbohydrate
Fetal
Lamina propria
Strong
Bone marrow
(+)
(+)
IgG
Protein
Neonatal
2nd lymphoid organ
Q:36:-Positive selection?
Ans:-In thymus cortex, the double positive thymocytes that bind to self MHC-I, -II molecules of
epitheliums in a proper affinity may develop further, but that in high affinity or no binding
will be removed.
Q:37:-Negative selection?
Ans:-In medulla of thymus, any thymocyte that binds tightly to self-Ag-MHC of an APC with
TCR will be removed, but that binds loosely or does not bind will survive.
Q:38:-Features of αβT & γδT cells?
Classify Basis
TCR
CO=receptor
Function
Subpopulations
αβT ;
γδT
+
+
CD4 T ; CD8 T
Th: Th1, Th2, Th17
CTL(Tc)
Treg ; nTreg , iTreg
Native T ; Effect T ; Memory T
Act State
Q:39:-APC?
Ans:-APC: Refer to the cells that can process Ag, and
present the Ag to T cells . [Two Types] ;
1. Professional APC: -Ag presentation.-Immune responses (Immune cells).2. Non-professional
APC: -Ag presentation (Non-immune cells).
Q:40:-Ag Processing?
Ans:-APCs digest taken up Ag
into peptide fragment of proper size so as to load the fragment
onto a Ag-binding cleft of a MHC molecule, and then present the Ag peptide-MHC complex on
surface of APC .
Q:41:-Ag Presentation?
Ans:-Refer to the process that during APC-T cell interaction, APC presents Ag peptide
cell by using its MHC molecule.
Q:42:-Comparison of Immature DCs with Mature DCs?
Immature
FcR
PRR
MHC II
Accessory Mol.
Ag uptake & processing
Ag presentation
Migrate to
High
High
Low
Low
Strong
Weak
Inflammatory tissue
Mature
Low
Low
High
High
Weak
Strong
2nd lymphoid tissue
to T
Q:43:-Immunological Synapse?
Ans:-Refer to the interface between a T cell and an APC. The key molecules are a group of
TCR-pMHC that are surrounded by CAMs.
Q:44:-Functions of Th1 & Th2 ?
Ans:-Functions of Th1:(1)Promote Mf to Kill Pathogens;- Mf Activating By secreting IFN-γ,
expressing CD40L -- Promoting Mf Proliferation & Differentiation: By secreting IL-3 etc. for
HSCs differentiation. - Chemotaxis on Mf to Inflammatory Site: By secreting TNF-α etc. to
promote the exudation of Mf.2) Activate Lymphocytes;-Th1 self act/prolifer/diff：e.g.IL-2.
-Tc act/prolifer/diff: e.g.IFN-γ/IL-2.-B act & produce opsonizing Ab: e.g.IFN-γactivate B cell to
secret IgG2a, a opsonin.(3) Promote Neutrophil to Kill Pathogens;-Th1 secrets TNF to activate
neutrophil, and to promote its phagocytotic and killing effects.Fuctions of Th2:(1)Help B cell
mediated humoral imm:- B activation/proliferation/differentiation /Ab production.(2)Involve in
Hypersensitivity：- Activate Mast cell/basophil/eosinophil to mediate hypersensitivity. B cell
differentiate to IgE-producing cell.(3)Anti-Parasite Effects： Eosinophil
activation/proliferation/ enhancing its killing activity.
Q:45:-The Target Cell Killing Pathway of Tc?
Ans:-(1)Porforin(Pf)/Granzyme(Gz)Pathway; -Secret Pf to destroy cell membrane.
-Secret Gz to induce apoptosis.(2)Fas / FasL Pathway;-Expressed FasL binds Fas to induce
apoptosis. -Secreted TNF binds TNFR to induce apoptosis.
Q:46:-Ig class switching?
Ans:-In immune responses, a B cell express IgM first, and then its
Ig gene keep the same V
region but rearrange C region genes so as to express other classes of Igs.- Happen after Ag
stimulation.- Regulated by CKs.
Q:47:-What is Ig Affinity Maturation?
Ans:- - An Ag can activate multiple clones with the same specific but
different affinity to
produce Abs with different affinity. - The Abs response and reduce the Ags.
- The clones with higher affinity can get the Ag and thus to produce the Abs preferentially.
Q:48:-Characteristics of the Secondary Humoral Responses?
Ans:-(1)Time lag shorter.(2)Abs increase rapidly.(3)Abs last longer .(4)Need less Ags to
stimulate.(5)Higher Ab affinity.
Q:49:-What are the innate immune cells?
Ans:->)Phagocytes; -Neutrophils -mononuclear phagocytes >)NK cells (Natural killer cells).
>)Dendritic cells.
Q:50:-The main functions of phagocytes and NK?
Ans:-Functions of phagocytes;i)To engulf and kill the invading pathogens.
ii)Participate and promote inflammatory reaction; -proinflammatory cytokine;- TNF-a、IL-1、
IL-6、IL-8、MIP-1a/b、MCP-1 ----Other inflammatory mediator ;- prostaglandin leukotriene
iii)Kill target cells; -ADCC -TNF-a iv)Ag processing and presentation; -present Ag--------T
cell activation v)Immunological regulation; -secret CKs----regulate other immune cells activity.
Functions of NK cells: i)Kill target cells; -tumor cell -virus infected cell -fungus
ii)Immunological regulation; -Secretion of cytokines , e.g. IFN-γ 、TNF-α、GM-CSF、IL-3 -----------to activate macrophages 、T、B、APC
Q:51:-Receptors of macrophage and their ligands?
Ans:-1) PRR and PAMP;i)Pattern Recognition Receptor (PRR); >)mannose receptor，MR >)scavenger receptor，SR
>)toll-like receptor ，TLR -Membrane PRR. -Secreted PRR.ii)Pathogen-Associated Molecular
Patterns , PAMP;-(Depending on PAMP innate immune system can distinguish self from non
self.)-LPS (lipopolysaccharide): from G- bacteria.-Lipoteichoic acid: from G- bacteria.
-Mannan: from various microbes, e.g.yeast.-Glycolipid: from mycobacteria.
3)Opsonizing receptors; ① FcγR---Ig Fc ② CR----C3b、C4b 4)Cytokine receptors;
-MCP-1, MIP-1α/β---chemotaxis , -IFN-γ. M-CSF, GM-CSF---activation.
Q:52:-Receptors of NK cell and their functions. The mechanism of
activating & inhibitory receptor work?
Ans:-Receptors of NK cell & their functions;-1)Nk cell receptors bind with MHC-I molecule:
--KIR(killer immunoglobin-like receptors):CYTOPLASMIC REGION..:- >Longer-an inhibitory
receptor.>Shorter-non-covalent combination with DAP-12(ITAM), an activating receptor.
--KLR(killer lectin-like receptor): >CD94: short cytoplastic region, no signal transmission
>NKG2A: ITIM in cytoplastic region --------CD94/NKG2A, an inhibitory receptor
>NKG2C: no signal transmission, bind with DAP-12(ITAM) ----CD94/NKG2C, an activating
receptor 2)NK cell activating receptors bind with non MHC-I molecule;=
--NKG2D ;- >Express mainly on the surface of NK and γδT
>No signal transmission , >Non-covalent binding with DAP-10(ITAM) .
--Natural cytotoxic receptor(NCR);-> NKp46,NKp30,NKp44
>Bind with CD3ζ-ζor DAP-12 (ITAM) ,>Kill target cells when KIR/KLR lose their function.
3)FcγR:- -Binding to the Fc of an antibody molecule.-Activate NK cells to kill the Ab-binding
target cell., -Mediate acquired immune response .
Mechanism of activating & inhibitory receptor work:1)The activating receptor activating the cell need meet two necessary conditions: ① Ligand
binding ② The signals of inhibitory receptors are inhibited.2)After inhibitory receptor
binding to self normal class I HLA molecules, the signal of activating receptors are inhibited
effectively and NK cells can’t be activated. 3)When HLA-I molecule losing or decreasing the cell
will become into target cell. the NK cells can be activated and kill him.
Q:53:-Relationship between innate immunity and adaptive immunity?
Ans:-1)Innate immune response switches on adaptive immune response:- DC &M supply the
first signal and second signal of T cells activation.2)Innate immune response affects the type of
adaptive immune response:- After getting stimulation of intracellular parasitic bacteria,M
produce IL-12 and IFN- γ . IL-12 and IFN-γ induce naive T cells develop to Th1 cells, which
can switch on cell-mediated immune response.If NKTs and mast cells getting simulation of
parasite, they produce IL-4, which can induce naive T cells develop to Th2 cells. Th2 cells switch
on humoral immune response.3)Innate immune response helps adaptive immune response educe
immunological effect.L:- Humoral immunity Ab Cell-mediated immunity complement、
opsonization、ADCC Th1
activate M
Q:54:-The features of innate immunity?
Ans:-1)Innate immunity is non-specific reactions:- >M, DC use PRR , to recognize PAMP
>To
all the infectious microbes & other things (non-self).2)No program of clone amplification.3)The
responses of innate immunity effect instantl:- -the first reactions of defense.4)No tolerance and
memory:- -no changes with reaction times.
Q:55:-Concept of Autoimmunity, Autoimmune Disease and Immunodeficiency
disease?
Ans:-Autoimmunity: is defined as an acquired immune reactivity against self antigens. This
response usually produces autoimmune antibody and autoreactive T cells .Autoimmune disease :autoimmune response lead to tissue damage.Immunodeficiency disease:- is characterized by the
progressive loss or depression of immune function caused by congenital hypoplasia or postnatal
factors.
Q:56:-The common diseases of autoimmune disease and of immunodeficiency
disease?
Ans:-Disease of autoimmune diseases:- 1)Graves’ Disease- stimulating Abs against receptor .
2)Myasthenia Gravis- Blocking Abs against receptor . 3)Goodpastur’s Syndrome-Extracellular
composition autoantibodies . 4)Diabetes-“ T cell” Disease Multiple Sclerosis .5)Systemic lupus
erythematosus ,SLE . 6) rheumatoid arthritis (RA). Diseases of immunodeficiency diseases:Primary immunodeficiency disease (PIDD) :- >Deficiency or combined deficiency of T ＆ B
cell DiGeorge syndrome , IgA deficiency , Severe combined immunodeficiency disease (SCID)
>Complement deficiencies, >Phagocytic defects.Secondary immunodeficiency disease (SIDD) :>Immunodecifiency caused by infectious agents :- Many bacterial, viral and parasitic agents
compromise the host immune functions, most prominent among theses is HIV infection.
>Immunodeficiency resulting from aging and malnutrition :- A number of immune functions
become less efficient with aging. >Immunodeficiency during malignancy and other diseases
Q:57:-The classification of AID and IDD?
Ans:-AID classification :ORGAN-SPECIFIC AUTOIMMUNE
DISEASES.
Type 1 diabetes mellitus
Goodpasture’s syndrome
Multiple sclerosis
SYSTEMIC AUTOIMMUNE DISEASES
Rheumatoid arthritis
Scleroderma
Systemic lupus erythematosus
Primary Sjogren’s syndrome
polymyositis
Grave’s disease
Hashimoto’s thyroiditis
Autoimmune pernicious anemia
Autoimmune addison’s disease
Vitiligo
Myasthenia gravis
IDD classification :- Primary immunodeficiency disease (PIDD) ; Inherited
immunodeficiencies Secondary immunodeficiency disease (SIDD) ; immunodeficiency
resulting from infections and other diseases. immunodeficiency resulting from iatrogenic 医源性
causes. immunodeficiency due to aging or malnutrition.
Q:58:-Clinical features of AID and IDD?
Ans:- AID :->The prevention and control of microbial infection (ex: diabetes mellitus)
>Application of immunosuppressive Medication(ex: corticosteroids, cyclosporin, methotrexate).
>Therapeutic Antibodies against specific T cell or cytokines ＆CKR (with fewer side effects)
Anti-CD4 McAb/IL-2R α chain.IDD:- >Recurrent infection; Severe infection .Refractory
infection .Recurrent infection .Opportunistic pathogens infection .Recurrent diarrhea
>High risk of autoimmune diseases >High risk of malignancy >Inherited tendency Genetic
correlation
Q:59:-Principle of antigen-antibody reaction?
Ans:-1)Specificity, 2)Reversibility ;weak non-covalent interactions. 3)Visibility, 4)Ag-Ab
reaction have two stages
Q:60:-Agglutination?
Ans:-Granular Ag or Ag attached on granules can bind with corresponding Ab, followed with
the formation of agglutinated clots, which is called agglutination reaction.
Q:61:-Precipitation?
Ans:-Soluble antigen ( exotoxin , serum protein, and exudation) combine with specific Ab in
appropriate condition would form visible precipitation ,this reaction is called precipitation
reaction. The reaction can be performed in fluid or semisolid medium such as agar.
In agar diffusion test including : .Single agar diffusion test, .Double agar diffusion test
Q:62:-Specificity?
Ans:-The ability of an antigen-bining site to react with only one antigenic determinant.
possibility of negative findings when negative patients are checked with immunodetection assay.
Specificity=true negative /(true negative +false positive ) ×100％
Q:63:-Sensitivity?
Ans:-Possibility of positive findings when patients are checked with immunodetection assay.
Sensitivity=true positive /(true positive + false negative ) ×100％
Q:64:-Modes about adaptive immunity?
Ans:-----------Immunity ----------------Natural(Innate)
-----------Acquired-----------------Passive----Artificial
Natural
-------Active------Artificial
Natural
Q:65:-Vaccine?
Ans:-Definition: is a kind of pathogen which is treated by human and used to elicit the
protective immunity to this pathogen. Basic Requirements of vaccine: safety, utility and
efficiency.
Q:66:-Artificial active immunity?
Ans:-A method that body obtains specific immunity to defense infection after inoculating
vaccine. There are three kinds of vaccine: killed vaccine (inactivated vaccine) , living vaccine
(attenuated vaccine) and DNA vaccine.
Q:67:-Artificial passive immunity?
Ans:-Give the human Abs or other CKs, which can help human defend the pathogenic organism
infection. It is a method that sustains short time. Including;>Antitoxin>Human immunoglobulin
>CKs >Monoclonal antibody , et al.
Q:68:-The difference between artificial active and passive immunity?
Item
Artificial active
Artificail passive
immunity
immunity
Inoculum
antigen
Ab, CK
frequency
1-3 times
1 time
Time of becoming
2-3 weeks
Immediately
effective.
Keep time
Few months - years
2-3 weeks
Main usage
Prophylaxis
Cure & urgent prophylaxis
Q:69:-Adjuvant?
Ans:-A nonspecific immune substance that can enhance immune response when combine with
antigen. Pre-input or co-input with antigen to organism can accentuate immune response or
change the type of immune response .
Q:70:-Immunolabeling Technique?
Ans:-Antigen or antibody labelled with marker (et al) is performed antigen-antibody reaction,
and we can detect these makers to know the condition of Ag-Ab reaction. These assays are the
most popular applicated immunotechnique.
Q:71:-Features of Ag-Ab reaction in vitro?
Ans:-Features of Ag-Ab reaction in vitro ;1)High degree specificity 2)Reversibility
3)Proportionality (visibility ) 4)Two phases of Ag-Ab reaction ; i)specific binding phase
ii)visible reaction phase
Q:72:-Immunological tolerance definition and feature?
Ans:-These antigen specific T cells and B cells can not be activated to induce immune response
under stimulation of Ag. This phenomenon is called immunological tolerance. Tolerogen:
antigens that induce tolerance.Features:>Only play tolerance to definite Ag, but play good
immune response to other Ags. (immunologically specific) >Only adaptive immunity has
tolerance. >Normal individuals are tolerant of their own antigens(self antigen)----- Selftolerance.
Q:73:-Comparison of T cell tolerance with B cell tolerance?
Ans:- Contents
T cell
B cell
=====================================================================================
Tolerance formation
easy
difficult
Antigens
TD -Ag
TD- Ag and TI –Ag
Dose of antigens
high or low
high
Induced time
shorter (1-2 days)
longer (more than 10 days)
Maintaining time
longer (a few months)
shorter (a few weeks)
Q:74:-Mechanism of central tolerance and periphery tolerance?
Ans:- Central tolerance: T cell central tolerance : formation in thymus ; >clonal deletion in
negative selection . B cell central tolerance: formation in bone marrow ; >clonal deletion
>clonal anergy (clonal inactivation) >receptor editing Periphery tolerance:- 1)Clonal deletion
and Immunological ignorance >Clonal deletion;-self Ag at high concentration and affinity can
induce self-reactive T cells clonal deletion. >Immunological ignorance ; self Ag at low
concentration or affinity can induce self-reactive T cells clonal ignorance. When Ag
concentration increasing , this tolerance can be stopped. 2)Clonal anergy. 3)The function of
regulatory T cells, (CD4+CD25+T、Tr1、Th3);
Treg
Cell-cell contacting
CK（IL-10,TGF-β
Inhibit T cell response
4)Function of CKs .
5)Disorder of signal transduction .
Q:75:-Definition and features of Immunoregulation?
Ans:-During the process of immune response, many immune molecules and immunocytes play
reaction each other to enhance or inhibit immune response. The negative and positive reactions
build a regulation net. Under the control of genetic gene, this net help us finish immune function
to antigen. Features:- i)The perception to the immunoresponse is the premise of immunoregulation.
ii)The mainstream of immunoregulation is negative feedback. iii)The immunoregulation do not
like immune intervention which is artificial, but is physiological feedback. iv)The disorder of
immunoregulation can induce diseases.
Q;76:-Internal image of Ag?
Ans:-The structure of Ab2 is similar with epitope of Ag and it can bind to CDR of Ab1 as same
as Ag. So we call this Ab2 internal image of Ag.
Q;77:-Which molecules can induce negative feedback of immunoresponse?
Ans:- TLR(PRR) recognizing PAMP induces immunoresponse through activating the signal of
MF-κB and MAP. The signal can be inhibited by PI3K and other molecules. Effector phase:
PI3K inhibit the immunoresponse activated by TLR-PAMP Tolerance phase: IRAK-M, SOCS-1
and others inhibit the immunoresponse activated by inflammatory mediator, such as LPS.
Q:78:-The inhibitory receptors on the T and B cells?
Ans:-B cells inhibitory receptors:-FcRII-B, CD22, CD72 T cells inhibitory receptors:CTLA-4, PD-1,
Q:79:-Hypersensitivity?
Ans:-Hypersensitivity (allergy): when an Ag invading body, immunity response is induced to
eliminate Ag. But in some case, body re-exposure to Ag again, as soon as immunity response
eliminate Ag, host’s tissue appears physiologic function disorder or even damaged by the response.
This abnormal response is termed hypersensitivity or allergy.
Q;80:-Types of hypersensitivity?
Ans:->Type I Hypersensitivity-Due to IgE binding to Fc receptors on mast cells and basophils.
>Type II Hypersensitivity-Due to antibody (IgG and IgM) mediated activation of complement or
antibody dependent cell mediated cytotoxicity (ADCC). >Type III Hypersensitivity-Due to
accumulation of immune complexes and the resulting inflammatory response. >Type IV
Hypersensitivity -Due to activation of TDTH cell mediated effectors
Q:82:-The treatment of type I hypersensitivity reaction?
Ans:-1)Find allergen and avoid touching. Skin Tests (P-K test)-Individual is inoculated with
allergen by scraping or Injection . Fast: results within 30 min.2)Acute desensitization.
Protocol：small dose (0.1ml,0.2ml,0.3ml),short time（20-30 min）,injection many times.
Principal: induce degranulation of limited allergize target cells. Application: need antitox serum
to save life but sensitive to it. 3.chronic desensitization protocol：microamount (g、ng)，long
time, multiple subcuntaneous injections. principle: change the allergen invading way. Induce Ab
class swithing. application: sensitive to known but not avoiding allergens
Q:83:-The typical disease of type I,II,III,IV reaction?
Ans:-Type I:- >Generalized anaphylaxis (Systemic anaphylaxis) :tetanus . >Respiratory
anaphylaxis :- Asthma , allergic coryza ,Pollen, dust . >Digestive tract anaphylaxis :-Allergic
gastroenteritis >skin :- Cnidosis , atopic dermatitis , utricaria(hives) , eczema.Type II:1)Blood transfusion reactions:-Transfused cells are killed by complement-mediated lysis.
Symptoms: Fever, chills, nausea, clotting within vessels and lower back pain. 2)Hemolytic disease
of the newborn. 4) post-streptococcal glomerulonephritis. 5) Goodpasture’s symdrome.
6)Grave disease (thyrotropic-stimulation hormone, TSH), high level thyrine. Type III:1) Local immune complex disease ..i)Arthus reaction ii)Human local immune complex disease.
2)General immune complex disease i)serum disease. ii)Systemic lupus erythematosus (SLE) .
iii)Rheumatoid arthritis. Iv)Post-streptococcal glomerulonephritis.
Type IV:- i)Infectious disease. ii)Contact dermatitis.
Q:81:-The mechanisms of type I,II,III,IV reaction?
Ans:-type I mechanism..: Allergen Stimulation ..Atopic individual
Produce FcR I Ag specific
IgE Invading again + Allergize target cells .. Mast cells ,Basophiles FcR I cross-linkage
degranulation Produce and secret mediators….Biological mediators
Smooth-muscle contraction Increased vascular permeability Mucus secretion
Diseases
(I). Allergize stage (II). Provocation stage (III). Effector stage Type II mechanism:-1.Ag - on
the surface of cells2.Ab – IgG and IgM；3.Cell damaged by complement, macrophage, NK cell et
al. Type III mechanism:-1)Ag: soluble Ag.2)Ab: IgG &IgM. 3)Immune complex. >Big size IC:
phagocytosis >Medium size: deposit >Small size: clear with urine 4)Tissue damage ; Complement,
neutrophiles, platelet et al.
Type IV mechanism:Antigen Inducing T cell (CD4+,CD8+)
Cytokine
Monocyte infiltration
Il-2
CD4+ T cell
IFN-γ
T cell proliferation
TNF-β
TF
Re-exposure
Tissue lesion
Exudation
MCF
MIF
cytotoxicity
Sensitized T cell
(CD4+,CD8+)
CD8+ T cell
Killing target cell