heavy chain

light chain

variable region (V area)

constant region (Zone C)

Location: between CH1 and CH2

Composition characteristics: Proline residue ↑→Hydrogen bond ↓→Easy to stretch and bend→Easy to change the distance between Y-shaped arms→Both arms bind BCR at different positions at the same time

Binding process: antigen + antibody → allostery between CH1 and CH2 of Ig molecule → exposure of complement binding site of Ig

Easily degraded: sensitive to proteases

IgM, IgE without hinge region

Connecting chain (J chain)

secretory patch (SP)

L chain: 2 functional areas—VL, CL

H chain

V region specifically recognizes and binds antigens

CL CH1: Ig genetic marker → there are differences in amino acids between different individuals

CH2 of IgG and CH3 of IgM: complement binding site → initiates the classical complement pathway; CH2 of IgG: related to crossing the placental barrier

CH3 of IgG, CH2 and CH3 of IgE: Cytophilic → binds to Fc receptors on a variety of cell surfaces

Point of action: near the N-terminus of the disulfide bond between the two heavy chains in the IgG hinge region

Effect: Ig→Fab*2 Fc

Point of action: near the C-terminal side of the disulfide bond between the two heavy chains in the IgG hinge region

Effect: Ig→F(ab')2 multiple pFc'

Gm of IgG; Am of IgA; Em of IgE; kappa light chain Km

Allogeneic, allogeneic, autologous→specific immune response→idiotypic antibody (AId)

Each Fab of Ig molecule contains 5-6 unique bits

In vivo: Inhibit bacterial adhesion, neutralize viruses, neutralize toxins → immune defense

In vitro: agglutination, precipitation reaction → immunological detection

Classic pathway: IgG1~3, IgM antigen→antigen-antibody complex→antibody configuration change→exposure of CH2 and CH3 functional region complement binding sites→C1q→activation of the classical pathway

Alternative pathway: activated by condensates of IgG4, IgA, and IgE

conditioning effect

ADCC (antibody-dependent cell-mediated cytotoxicity)

Mediates type I hypersensitivity reactions

IgG nascent Fc receptor (FcRn, located on the surface of maternal trophoblast cells in the placenta) → IgG is transferred into the trophoblast cells → cells are effluxed and enters the fetal blood circulation → the fetus passively acquires specific immunity

IgA Fc Polymeric immunoglobulin receptor (pIgR, expressed on the basal surface of mucosal epithelial cells) → Mucosal cell transport body → Mucosal surface-pIgR cleavage → sIgA is located on the mucosal surface (SP delays IgA degradation)

Plasma cells (spleen, lymph nodes) synthesize and secrete

Existence form: single body

Subclasses: IgG1 IgG2 IgG3 IgG4

Synthesis time: begins 3 months after birth

Serum 50% (accounting for 70% of total Ig in serum), extracellular fluid 50%

Anti-infection: Neutralizes exotoxin toxicity

Immune response: IgG1-3 forms immune complexes; activates complement through the classical pathway (bacteria, cytolysis); opsonization; ADCC effect

Infant's natural passive immunity: can cross the placenta

Pathology: Multiple autoantibodies ∈ IgG → participate in autoimmune reactions; IIIII hypersensitivity reactions

Another name: Macroglobulin (the largest among the 5 types of Ig molecules)

Existing form: pentamer (10 antigen binding sites)

Monomeric expression form: membrane protein (BCR)

In serum (accounting for 5%-10% of total serum Ig)

Antimicrobial: Antigen binding site ↑ → Strong binding to pathogens → Highly effective antimicrobial antibodies

Anti-infection: Neutralizes toxins and viruses

immune response

Type II and III hypersensitivity reactions

other

Synthesis by plasma cells (lymph nodes enter the bone marrow after activation and differentiation)

Existence form: single body

Half-life: 5-6 days

distributed

effect

Plasma cells (lamina propria of mucosa: respiratory tract, digestive tract, urogenital tract)

exist

effect

Type I hypersensitivity reaction

antiparasitic immunity

Advantages: wide source, easy to prepare

Disadvantages: low specificity, easy to cross-react, difficult to prepare in large quantities

Mouse splenocytes (specific B cells) myeloma cells (immortal proliferation) → hybridoma - massive expansion and immortality

Antigen detection: tumor antigens, cell surface antigens and receptors, hormones, neurotransmitters, cytokines...

Tumor localization diagnosis, immune-guided therapy: mAb radioactive substance/anticancer drug/toxin conjugation

Preventing and treating organ transplant rejection: anti-T cell mAbs

Advantages: high purity, high specificity, high potency, little or no cross-reaction, and can be mass produced

Disadvantages: mouse-derived mAb → hypersensitivity reaction

Cutting, splicing and modifying Ig→new type of antibody

Human-mouse chimeric antibody: mouse antibody V region, human antibody C region → mouse-derived specificity, affinity ↑ human low immunogenicity ↓, antibody type conversion

Modified antibody (humanized antibody): mouse CDR, remaining human Ig part → Immunogenicity ↓↓

Small molecule antibody: Fab/Fv (VH VL)/single peptide chain → immunogenicity ↓, penetrating property ↑

Bispecific antibodies: two different antigen binding sites

other