ABCT 101 · Immunology L1 · Basic concept of Immunology

📚 Immunology Lecture 1 · Basic concept of Immunology ABCT 5101 · 21 Oct 2026

Three lines of defence, two immune systems, and one recognition mechanism. The lecture answers a single question in three stages: what the system is, where it happens, and how it tells friend from foe.

5101 · IMM-L1 Basic Concepts of Immunology — 免疫學基本概念

ABCT 5101 Immunology Part Lectures · Lecture 1 · 21 Oct 2026. The lecturer's own annotated notes carry the section letters A–G; they are kept below so you can find any point on paper. Everything in the body is what was written on the board — the numbers, the lists and the wording are the lecturer's, not reconstructed.

How this lecture is built Three definitions → three lines of defence → the organs that do the work → two systems (innate vs adaptive) → how each one recognises a pathogen (PAMP / DAMP / PRR) → the barriers and the phagocytes that execute the response. Section letters: A definitions · B three lines of defence · C key features & players · E lymphoid organs · G innate vs adaptive. D and F were section headings the lecturer left blank.

Master Logic 主線邏輯 — the immune system as a three-layer national defence

  • Outside world (pathogens, toxins, pollutants) vs inside world (cancer cells, transplanted tissue) — the system must answer both, and only the inside half is unique to this course's framing.
  • First line = epithelium and skin, present from birth, non-specific.
  • Second line = innate immunity — fast, non-specific, no memory, but it destroys the pathogen before it has been identified, and in parallel it stimulates adaptive immunity.
  • Third line = adaptive immunity — antigen-specific, slow (days–weeks), and the only line with immunological memory.
  • Both are needed — the lecturer's note: "We need to have both of them in our body to eliminate the pathogens or NON-SELF cells."

A · Three definitions 三個核心定義

TermLecturer's definition
ImmunologyStudy of the components and functions of the immune system of an organism — a host-defence mechanism study.
ImmunityAbility of the host [human] to protect itself/herself against foreign organisms / substances — bacteria, virus, fungi, parasites — or abnormal cells (e.g. cancer cells).
Immune systemProtects us from physical, chemical and biological invasion; against bacteria, virus, fungi, parasites, toxin, pollutants; and against abnormal cells (cancer cells, tissue transplantation).
Exam focus — the two worlds The lecturer's own bracketing, worth reproducing verbatim in an answer:
• defence against the "OUTSIDE" world → pathogens, toxins, pollutants
• defence against the "INSIDE" world → cancer cells, tissue transplantation

Note the word host-defence on the Immunology line: it is what makes this a defence subject rather than a disease subject.

B · Three lines of defence 三道防線

LineWhat the lecturer wrote
1 First line of defenceEpithelial linings of those parts of the body in contact with the environment (outside). Example: skin cells.
2 Second line of defenceNon-specific host defence mechanism that comprise the growth and survival of pathogenic micro-organisms — i.e. innate immunity.
3 Third line of defenceSpecific immune system against invasion of foreign and local abnormal cells & substances — i.e. adaptive immunity.
What the immune system is important for Seven items, exactly as listed: 1. Inflammation · 2. Infectious diseases · 3. Tumour immunity · 4. Auto-immune diseases · 5. Allergy · 6. Vaccination · 7. Organ transplantation … etc.

Items 3, 6 and 7 are the ones that matter commercially: tumour immunity is the whole immunotherapy market, vaccination is the platform business, and transplantation is what sets the immunosuppression market.

The lecturer's warning, in blue ink "Immune system is NOT just about the infectious diseases." If you answer an immunology question with only infection in mind, you have answered half of it.

C · Key features and key players of the immune system

Three features define it: recognition (self vs non-self) → specificity of the response → immunological memory.

FeatureMeaning as written
Ability to distinguish between "SELF" and "NON-SELF"→ Recognition. This is the premise the whole PAMP argument rests on: a PAMP is absent from human cells because this discrimination has to work.
Specificity of the immune responseNot every response is generic — the adaptive arm targets one antigen.
Immunological memoryThe property that makes vaccination and booster doses work at all.

Key players = the major immune organs / tissues / cells. The lecturer's definition of the term itself: refer to those tissues / organs in which maturation, differentiation and proliferation of the immune cells take place.

Memory frame Primary lymphoid organs = military academy (T cells graduate in the thymus, B cells in the bone marrow). Secondary lymphoid organs = border checkpoints (pathogens are filtered, inspected and destroyed on entry).

E · Major organs and systems 淋巴器官

#OrganClass
1ThymusPrimary lymphoid organs — "Lymphopoiesis" (white blood cell to make)
2Bone marrow
3TonsilsSecondary lymphoid organs / tissues — "Effector mechanisms" (removal of microbial cells; immune cell proliferation / development)
4Adenoids
5Spleen
6Lymph node
7Mucosal lymphoid system — connected together lymphatic system

E1 · Primary lymphoid organs 初級淋巴器官

Two organs. Both are where immune cells are made; the bone marrow supplies the stem cells, the thymus finishes the T cells.

[1] Thymus — located near the neck region.
Functions: [1] production of lymphocytes; [2] major site of maturation of T-cells.

[2] Bone marrow — located in the long bones [e.g. femur, sternum and spine]; the lecturer counts 6 major sites for the production of immune cells.
Function: consists of various hematopoietic stem cells [HSC] which give rise to different types of blood cells and immune cells by hematopoiesis.

Hematopoiesis 造血作用 — memorise the definition • the formation and development of blood cells (including red blood cells & WBC)
• all blood cells are derived from hematopoietic stem cells [HSC]
• it occurs in bone marrow

WBC = white blood cells. The trap: bone marrow does not only make red cells. Every blood cell — red and white — comes from HSC.

E2 · Secondary lymphoid organs 次級淋巴器官

[1] Tonsils 扁桃腺 — located near the oropharynx and nasopharynx.
Functions: [1] tonsils reach their largest size near puberty; [2] production of lymphocytes; [3] prevent entry of pathogens through the nasal and oral route; [4] production of immunoglobulins [antibody]; [5] fight off infection.

[2] Adenoid 腺樣體 — located behind the nasal cavity.
Functions: [1] production of antibody; [2] provide local immune protection; [3] undergo atrophy by puberty.

The classic confusion Tonsils are largest near puberty. Adenoids atrophy by puberty. They are opposite trajectories, and the exam has used the swap as a distractor.

[3] Spleen 脾臟 — located under the ribcage and above the stomach in the left upper quadrant of the abdomen; one of the largest organs in the lymphatic system.
Functions: [1] production of WBC and antibodies (helps to fight infection); [2] filter blood to get rid of old and damaged blood cells; [3] production of red blood cells [RBC]; [4] blood storage organ.

[4] Lymph node 淋巴結 — located throughout the entire body, but mainly found in the neck, armpits, chest, abdomen and thigh regions.
Function: acts as a filter for foreign antigen [substances] — virus, bacteria, cancer cells, damaged cells etc.
Cell types: WBC (lymphocytes); B-cells; T-cells; macrophages; NK [Natural Killer] cells; Dendritic cells [DC] etc.

[5] Mucosal lymphoid system 黏膜淋巴系統 [MALT] — mucosal-associated lymphoid tissues, scattered along the mucosal lining in your body [submucosal membrane].
Examples: [1] gastrointestinal tract [G.I. tract] · [2] respiratory tract [R.T.] · [3] urogenital tract · [4] nasopharynx · [5] breast · [6] salivary gland system · [7] eye.
Functions: [1] fight off the foreign substances passing through the mucosal epithelium; [2] provide an important part in "local" immunity.

Sub-classFull nameSite
GALTGut-associated lymphoid tissuesG.I. tract — Peyer's patches link to the lymph node
BALTBronchial-associated lymphoid tissuesRespiratory tract
NALTNasal-associated lymphoid tissueNasopharynx

G · Two basic immune systems 兩大免疫系統

FeatureInnate immunity 先天免疫Adaptive (Acquired) immunity 適應性免疫
1 Inborn?Inborn — present from birthNOT inborn — learning / develop during the host lifetime
2 Always on?Always "ON"Requires activation
3 SpecificityNon-specific — responds in a generic way to all types of pathogens; defence is NOT examined with what the pathogen is; destroys pathogen before identificationHighly specific — specific response to different types of foreign substances, antigen-based; responds differentially
4 DurationNOT long lasting immunityLonger lasting
5 SpeedQuick / rapid response [mins–hours]; immediate activation after recognizing foreign substances (e.g. PAMPs / DAMPs)Response slower; delayed response — days to weeks
6 MemoryNo memoryHas memory — fast and strong on re-exposure
7 Key moleculesCytokines and complement proteinsCytokines and antibodies
8 Key cellsMacrophages, Neutrophils, Natural-Killer cells etc.B-cells & T-cells etc.
Which line of defence1st & 2nd line of immune system3rd line of defence
10 Clinical correlateInflammation · hypersensitivity · infectionVaccination · autoimmunity · tumour immunity · transplant rejection
The lecturer's summary of the two Innate immunity → working hand in hand. The note reads: innate immunity "stimulating adaptive immunity", and adaptive immunity is where antigen sits. The hand-drawn curve on the next sheet is the same statement in time: innate rises first and quickly, adaptive rises later but higher and longer — the picture of a booster response.

Key communication 細胞訊息傳遞

[1] Cytokines 細胞激素 — the "chemical messenger" in our immune system.
Small peptide cell-signalling molecules that aid "cell–cell communication" in our immune system and keep our immune system "functioning"; they stimulate the movement of immune cells toward the infection sites.
Involvement of immune cells — four pairings as written: [A] cell activation → immune response · [B] cell differentiation → immune cell development · [C] cell proliferation → immune response · [D] cell maturation → immune cell development.

[2] Antigen presenting cells [APC] 抗原呈遞細胞
Antigen: foreign substances [NON-SELF] stimulating the immune system.
APC: initiate adaptive immune response by presenting antigen captured from the environment / pathogens to adaptive immune cells [e.g. B-cells / T-cells].
APC examples: Macrophages (Mφ), Dendritic cells (DC).

Why the commercial industry cares about this step Antigen presentation is the hinge between innate and adaptive. Every checkpoint inhibitor and every cancer vaccine is an attempt to change what gets presented or whether it gets presented. APC biology is not background here — it is the mechanism of action.

Innate immunity 先天免疫 — the 1st line: external barriers 外部屏障

[1] Exogenous infection 外源性感染 — pathogen originating from a source outside the body (e.g. pathogens, toxins, allergens etc.).
Entry sites: skin, mucosal surface, ingestion, injection etc.

[2] Endogenous infection 內源性感染 — microbes already existing inside / on our body.
Examples: [1] opportunistic pathogens — normal flora in our body, which become pathogenic when your immune system is weakened; [2] antibiotic; [3] chemotherapy.   [2] Latent pathogen — dormant status.

Portals of entry 病原體入口 Pathogens / micro-organisms enter the host (body tissues) to cause infection. The lecturer numbered eight on the body diagram:
[1] Ear · [2] Conjunctiva of eye · [3] Nose · [4] Mouth · [5] Placenta · [6] Vagina / in males: penis · [7] Urethra · [8] Anus — plus broken skin and insect bite, which share the skin route.

[6] Types of external barriers 外部屏障三大類

TypeMembers as written
1 Physical barriersSkin epidermis; cilia
2 Chemical barriersFatty acid; low-pH chemicals; enzyme-based chemicals / proteins
3 Microbiological external barriersNormal flora (commensal flora)

[5] Physical barriers · [1] Skin epidermis 皮膚表皮 — three main layers:

LayerContents
EpidermisOutermost layer. The barrier itself: the lecturer's sketch labels it "tightly packed dead cells, keratinized cells [waterproof]" — and the consequence is written on the same line: "if no damage", pathogens cannot get in. The epidermis is constantly shed and replaced, removing microbes and pathogens.
DermisSweat gland, sebaceous gland; immune cells: macrophages etc.
Subcutaneous layerThe fatty layer below.

[5] Physical barriers · [2] Cilia 纖毛 — present in the respiratory tract mucosa. The chain as drawn: mucosa → produce mucus; the mucus traps unwanted materials; the outside cilia are "sweeping", so the trapped load is moved out. A mucus escalator, not a wall.

[1] Chemical barriers 化學屏障 — three groups, and this table is the one to memorise because the lecturer gave exact figures:

GroupMemberpH / detailFunction as written
Fatty acidSkin surface – sebum
produced by the sebaceous gland
pH ≈ 5.5Lower the skin pH to inhibit the growth of pathogen; prevent pathogen adhere on the surface of skin.
 
Low pH chemicalsStomach acidpH ≈ 2Ensure the condition is not suitable for the majority of the pathogen to grow.
Genitourinary tract – VaginapH ≈ 3.5 – 4.5Protect the host from bacterial infection.
Sebumsee fatty acid above.
Enzyme-based chemicals / proteinsTears, saliva, mucus — contain Lysozymes—Attack the surface layer of bacteria (peptidoglycan).
Gastric juice — contains Pepsin (protein)—A protein digestion enzyme in our GI tract; degrade the protein of pathogen.

[3] Microbiological barriers 微生物屏障 · Normal flora 正常菌群 — normal flora (commensal flora) colonize on the external interfaces of our body.
Examples: G.I. tract · respiratory tract · skin · mouth · vagina · eye.
Functions: [1] normal flora form a protective layer to prevent pathogens from colonizing and invading our body; [2] producing anti-microbial substances.

Why this is a commercial category, not a footnote The same mechanism read from the other side is the probiotic / live biotherapeutic market: you are manufacturing the protective layer on purpose. It is also why antibiotics can cause opportunistic infection — kill the flora, and the competitors move in.

Innate immunity — the 2nd line: cell (immune) and chemical

Phagocytosis 吞噬作用 — an important cellular processing and eliminating foreign particles (e.g. pathogens, foreign substances, damaged cells etc.).
It is the 2nd line of defence in innate immunity, against pathogens that have penetrated the 1st line of defence.

PlayersExamplesCharacteristics
Professional phagocytes[A] Macrophages [Mφ] · [B] Dendritic cells [DC] · [C] Neutrophils · [D] MonocytesCan rapidly be recruited to an injured or infected site via chemotaxis.
Non-professional phagocytes[1] Fibroblast · [2] Endothelial cells (blood vessel lining) · [3] Epithelial cells (G.I.T., respiratory tract etc.)Immobile; slower and less efficient phagocytic process compared to professional ones; limited in the range of particles (foreign substances) that can be engulfed.
Memory frame Professional = SWAT team (fast, chemotaxis, unlimited scope). Non-professional = bystander (immobile, slower, limited scope).

Adaptive immunity 適應性免疫

Cell-mediated immunity 細胞免疫 — the adaptive arm is executed by cells, not by soluble molecules. Details are covered in Lecture 2 (4 Nov).

How do immune cells recognise the pathogen 免疫細胞如何識別病原體

The central mechanism of the lecture. Innate cells read PAMPs on the pathogen and DAMPs released by your own damaged cells; adaptive cells read antigen. Both are detected by PRRs on the immune cell surface.

MoleculeFull nameComes fromRecognised by
PAMPsPathogen-Associated Molecular PatternsThe pathogen (bacteria, virus, fungi)PRRs → triggers innate immunity
DAMPsDamage-associated molecular patternsYour own dying, stressed or damaged cells — endogenous danger signalsPRRs → triggers innate immunity
Antigen—The pathogenThe adaptive receptors (BCR / TCR)
PRRsPathogen-recognition Receptors
written “pattern recognition receptors” on the standard spelling
Specialised receptors on the surface of immune cellsDetect the PAMPs and/or DAMPs

[1] DAMPs [Damage-associated molecular patterns]
• Endogenous signal — danger protein signal molecules released by dying cells, stressed, or damaged cells
• activation of innate immunity
• Example: [1] Heat shock protein [HSP] — released from stressed cells; it is a stress protein

[2] PAMPs [Pathogen-associated molecular patterns]
• only be found in the pathogen (e.g. bacteria, virus, fungi etc.)
• conserved molecular structure found on the surface or inside the pathogen

The five PAMPs — with their exact location
PAMPWhere it is
[1] Lipopolysaccharides [LPS]Outer membrane of Gram-negative bacterial cell wall
[2] PeptidoglycansCell wall of Gram-positive bacteria (major) and Gram-negative
[3] LipopeptideOn the surface of the plasma membrane of bacteria
[4] Unmethylated CpG DNABacterial / viral DNA containing the motif [CpG] — short sequence containing cytosine (C) and guanine (G)
[5] FlagellinStructural protein of bacteria flagella

The Gram-positive / Gram-negative diagram on that sheet is the reason LPS and peptidoglycan are listed separately: LPS sits on the outer membrane and is the classic Gram-negative signature, whereas peptidoglycan is the Gram-positive major component and is present in both.

Important characteristics of the PAMPs — five, all required [1] Unique structure present in microbes / pathogens
[2] are essential for the survival of pathogens
[3] Absent in human cells — the immune system can distinguish between "SELF" and "NON-SELF"
[4] can be recognized by PRRs (Pattern Recognition Receptors)
[5] trigger innate immune response

Characteristic [3] is the load-bearing one. If a PAMP were present on human cells, innate immunity could not tell friend from foe — which is exactly the requirement stated in section C.

[3] PRRs [Pathogen-recognition Receptors]
• specialised receptors of the innate immune system
• immune cells have these types of receptor to detect the pathogen or "NON-SELF" or damaged cells etc.
• detect the PAMPs and/or DAMPs

The lecturer drew three types of PRRs as a three-branch tree and labelled only the first branch — Type I: extra-cellular PRRs — before the sheet turned to TLRs. The other two branches were not filled in on the day.

Toll-like receptors [TLRs] — the Type I example the lecturer developed:
[1] TLR originally was found fruitfly [Drosophila]
[2] recognize PAMPs and DAMPs
[3] mainly associated with defence against bacteria, virus, fungal infection etc.
[4] activate signalling pathways → leading to production of cytokines / chemokines
[5] 10 different types of known TLRs (human)

TLR → what it reads
TLRLigand
TLR3, 7, 8RNA (viral)
TLR9Unmethylated CpG DNA (bacterial / viral DNA)
TLR4LPS (Gram-negative bacteria)
TLR2, 6Lipopeptides (bacteria)

The trap: TLRs are not only for bacteria. TLR3/7/8 read viral RNA and TLR9 reads viral DNA. 10 TLR types in human.

Page-by-page details from the handwritten Lecture 7 notes

After re-reading all 30 handwritten pages at full size, these are the details the note was missing or had only as a name. In a multiple-choice exam, these are exactly what separates the options.

1 · The lecturer's own numbering

LectureDateTitle
Lecture 1Oct 21Basic concept of Immunology
Lecture 2Nov 4Innate & Adaptive Immunity
Lecture 3Nov 11Immune system disorder
Different from the official timetable The official docx calls 21 Oct “L7”, 4 Nov “L8”, 11 Nov “L9”. The slides use 1 / 2 / 3, which is why this site labels them IMM-L1 / L2 / L3. Keep the two numbering systems apart.

2 · The three lines of defence, in his words (p4)

LineWhat the slide says
FirstEpithelial linings of the parts of the body in contact with the environment; e.g. skin cells
SecondA non-specific first defence mechanism that compromises the growth and survival of pathogenic micro-organisms
ThirdSpecific immunity against invasion of foreign and local abnormal cells and substances

The immune system is not only about infection — his list of seven: inflammation, infectious diseases, tumour immunity, autoimmune diseases, allergy, vaccination, organ transplantation.

3 · Three features + 3R (p5, p12–13)

Features: distinguish self / non-self, specificity, immunological memory.
Behaviour: 3R — Recognition → Respond → Resolve/Recover. His cartoon says it plainly: “hello” to self, “who r u?” to non-self, and in the end only the non-self is eliminated.

4 · Organs: what each one does (p6–p11)

OrganTypeFunctions listed
ThymusPrimaryProduction of lymphocytes; major site of T-cell maturation; near the neck
Bone marrowPrimaryLong bones (femur, sternum, spine); HSCs give rise to blood and immune cells by haematopoiesis
TonsilsSecondaryLargest near puberty; produce lymphocytes; prevent pathogen entry through nose and mouth; produce immunoglobulins
AdenoidSecondaryBehind the nasal cavity; antibody production, local protection; atrophies by puberty
SpleenSecondaryLeft upper abdomen above the stomach; filters blood, removes old red cells; makes WBC and antibody; blood storage
Lymph nodeSecondaryNeck, axilla, chest, abdomen, thigh; filters foreign antigen; contains B/T cells, macrophages, NK, DC
MALTSecondaryAlong mucosa; GALT (gut, with Peyer's patches), BALT (bronchial), NALT (nasopharynx); also urogenital, breast, salivary gland, eye
Exam point Primary = where immune cells mature (thymus, bone marrow); secondary = where the response happens (everything else). “Primary builds the army; secondary fights the war.”

5 · Portals of entry (p19)

Nine portals on his diagram: skin (including broken skin), conjunctiva of the eye, nose, mouth, placenta, vagina, urethra, anus, insect bite. That is why mucosa is the main battlefield of the first line.

6 · Exogenous vs endogenous infection (p18)

ExogenousEndogenous
SourceOutside the body: pathogens, toxins, allergensMicrobes already inside/on the body
EntrySkin, mucosa, ingestion, injection—
ExamplesFood poisoning, wound infectionOpportunistic normal flora when immunity drops; latent pathogens that reactivate

7 · The numbers behind the barriers (p20–p22)

TypeMechanismExamples / numbers
PhysicalTightly packed keratinised dead cells, constantly shed; cilia + mucus trap particlesThree skin layers (epidermis / dermis / subcutaneous); respiratory cilia
Chemical (fatty acid)Sebum from sebaceous glands stops pathogens adheringSkin surface
Chemical (low pH)Acid environment unsuitable for growthStomach pH ≈ 2; vagina pH ≈ 3.5–4.5; skin / serum pH ≈ 5.5
Chemical (enzymes)Lysozyme cleaves bacterial peptidoglycan; pepsin digests proteinTears, saliva, mucus; gastric juice
MicrobiologicalNormal (commensal) flora: occupy space, form a protective layer, produce antimicrobial substancesGI tract, respiratory tract, skin, mouth, vagina, eye

8 · The “cellular + chemical” list of line two (p23)

CellularChemical
Macrophages, neutrophils, mast cells, dendritic cells, NK cells, eosinophils, monocytesComplement (proteins, antimicrobial), cytokines (communication with adaptive immunity), inflammation / acute-phase proteins, lymph, blood

9 · Phagocytosis in three steps (p28–p29)

StepNameWhat happens
1RecognitionPAMPs on the pathogen are read by PRRs on the phagocyte
2RespondInternalisation begins, forming a phagosome
3ResolvePhagosome fuses with a lysosome → phagolysosome containing lysozyme, proteases, nucleases → killing → debris handed to adaptive immunity (Mφ as APC)

Professional vs non-professional phagocytes: professionals (Mφ, DC, neutrophil, monocyte) are recruited rapidly by chemotaxis; non-professionals (fibroblasts, endothelial cells, epithelial cells) are immotile, slower and limited in what they can engulf.

10 · Innate vs adaptive in nine lines (p14)

AspectInnateAdaptive
OriginInbornLearned during life
StateAlways ONInduced
SpecificityNon-specific (generic)Highly specific (antigen-based)
SpeedHoursDays to weeks
MemoryNoneYes (faster and stronger on re-exposure)
Key moleculesCytokines, complementAntibodies, cytokines
Key cellsMφ, neutrophils, NKB and T cells; APCs present antigen
LineFirst and secondThird
When it failsRecurrent infectionAllergy, autoimmunity

Kinetics (p17): innate peaks first → adaptive is induced → adaptive takes over → immunological memory. The response falls once the pathogen is cleared, but memory cells remain.

11 · Three definitions that get examined (p16, p30)

  • Cytokine: small peptide signalling molecules for cell–cell communication, attracting immune cells to the infection site; involved in activation, differentiation, proliferation and maturation.
  • Antigen-presenting cell (APC): captures antigen from the environment and presents it to adaptive immune cells (B/T); e.g. Mφ, DC.
  • DAMP: endogenous danger signal released by dying, stressed or damaged cells, activating innate immunity; e.g. heat shock protein (HSP).
One-line Summary English: The immune system defends the outside world (pathogens, toxins) and the inside world (cancer, transplant) through three lines — epithelium, non-specific innate, and specific adaptive — and it is not only about infection. Innate immunity reads PAMPs on the pathogen and DAMPs from your own stressed cells through PRRs (e.g. TLR4 = LPS), fast and without memory; adaptive immunity reads antigen, slowly but with memory. Both are required.
中文邏輯:免疫系統同時守外面(病原體、毒素)與裡面(癌細胞、移植組織),分三道防線——上皮、非特異先天、特異適應性;而且不只關乎感染。先天用 PRR(如 TLR4 = LPS)讀病原體的 PAMP 與自身受損細胞的 DAMP,快而無記憶;適應性讀抗原,慢而有記憶。兩者缺一不可。