1️⃣ Two Main Arms of Immunity

Innate Immunity = Fast + Non-specific

• First line → hours
• No memory
• Main cells → macrophages, neutrophils, NK cells
• Main proteins → complement
• Triggered by: common microbial patterns (PAMPs), damaged tissue DAMP

Adaptive Immunity = Slow + Specific

• Takes days
• Strong memory
• Main cells → T cells, B cells
• Activated by: antigen presentation by APCs

👉 Exam logic:

Innate = immediate, pattern-based

Adaptive = delayed, antigen-specific, memory-forming

2️⃣ Key Cells & Their Functions (Super High Yield)

🧱 A. Phagocytes (Innate)

Macrophages

• Long-lived, tissue-resident
• Receptors: Fcγ (IgG) + Complement (C3b)
• Functions:
• Phagocytose + kill microbes
• Present antigen to T cells → link innate ↔ adaptive
• Release cytokines (IL-1, TNF-α)

Neutrophils

• Most abundant WBC
• Short-lived (few days)
• Phagocytosis
• Kill by:
• Degranulation (enzymes, ROS)

Mast Cells & Basophils

• IgE-mediated degranulation
• Release histamine, prostaglandins, heparin
• Cause allergy + inflammation

Eosinophils

• Anti-parasite
• Attach to parasite → degranulate → toxic proteins → kill parasites

🧲 B. NK Cells = Innate + Adaptive Bridge

• Kill virus-infected + tumour cells
• Two receptors:
1. CD16 (FcγRIII) → binds IgG → ADCC
2. KIRs → sense absence of MHC-I → kill
• Activated by IL-2 & IFN-γ from T cells

👉 Logic:

Healthy cell = expresses MHC-I → NK inhibited

Diseased cell = low MHC-I → NK attack

3️⃣ Complement System – the Most Exam-Loved Topic

Major Functions

1. Lysis (MAC C5–C9)
2. Opsonisation → C3b coats bacteria → ↑ phagocytosis
3. Inflammation → C3a, C5a attract neutrophils (anaphylatoxins)

Three Activation Pathways

All pathways converge at:

👉 C3 cleavage → C5–C9 (MAC)

Clinical importance

• C3 deficiency → recurrent severe bacterial infections
• Classic pathway deficiency → autoimmune disorders

🚀 ADAPTIVE IMMUNE RESPONSE

Adaptive immunity = highly specific, has memory, long-lasting protection, mediated by B cells + T cells.

1️⃣ B CELLS — Antibody-mediated (Humoral) Immunity

What they do (high-yield):

• Develop in bone marrow
• Recognise extracellular antigens
• Present antigen on MHC-II to T helper cells
• Become plasma cells → produce antibodies
• Form memory B cells

👉 Logic:

B cell sees antigen → internalises → presents with MHC-II → T helper gives cytokines → B cell proliferates → plasma cell → antibodies.

2️⃣ ANTIBODIES (IMMUNOGLOBULINS) – ABSOLUTE MUST-KNOW

All antibodies = 2 light + 2 heavy chains

Fab = binds antigen

Fc = determines function (complement activation, opsonisation, placental transfer)

High-Yield Functions of Each Class

IgM

• First antibody in primary response
• Cannot cross placenta
• Pentamer → strongest complement activator
• Intravascular

IgG

• Most abundant (70–80%)
• Main antibody of secondary response
• Crosses placenta (IgG1, 3, 4) → fetal protection
• IgG1 & IgG3 → best complement activators + opsonisation

IgA

• Secretions (saliva, tears, GI, GU, breast milk)
• Mucosal protection by blocking microbial adhesion
• Dimer in secretions
• dimer

IgE

• Binds mast cells + basophils
• Cross-linking → allergic reactions
• Parasitic defence

IgD

• On B cell surface as a receptor
• No major serum role

👉 Memory tip:

M G A E D = MeGa Aunty Eats Doughnuts

(M = first; G = most; A = secretions; E = allergy; D = receptor)

3️⃣ VACCINATION — Why It Works

• Primary response produces memory B cells
• On re-exposure → massive, rapid IgG response
• Vaccines mimic infection without causing disease

👉 Key concept:

Vaccines keep epitopes intact but remove toxicity.

4️⃣ T CELLS — Cell-mediated Immunity

Develop: Bone marrow → thymus (selection)

Recognise antigen only when presented on MHC.

Types of T cell receptors

• αβ TCR → 95% of circulating T cells
• γδ TCR → mucosa; MHC-independent

5️⃣ THYMIC SELECTION — Extremely Exam-Loved

Positive selection

• Occurs in cortex
• TCR must recognise self-MHC → survive

Negative selection

• Occurs in medulla
• TCR binding too strongly to self-antigen → apoptosis
• Prevents autoimmunity

👉 Survivors become:

• CD4⁺ (Th cells) = MHC-II restricted
• CD8⁺ (Tc cells) = MHC-I restricted

6️⃣ CD4⁺ T CELLS (HELPER CELLS) — Commanders

Recognise antigen on MHC-II

Th1

• Produce IFN-γ, IL-2
• Activate macrophages
• Activate CD8⁺ cytotoxic T cells
• → Cell-mediated immunity

Th2

• Secrete IL-4, IL-5
• Activate B cells → antibodies
• → Humoral immunity

👉 Key polarising cytokines:

• IFN-γ + IL-12 → Th1
• IL-4, IL-5→ Th2

Other CD4 subsets (low yield but quick to remember)

• Th3 → ↑ TGF-β
• Th0 → both Th1 + Th2 cytokines
• Tr1 → ↑ IL-10 → immune suppression

7️⃣ CD8⁺ T CELLS (CYTOTOXIC T CELLS)

Recognise antigen on MHC-I

Functions:

• Kill virus-infected cells
• Kill tumour cells
• Release:
• Perforin → pores
• Granzymes → apoptosis

Types:

• Tc1 → driven by IL-12 + IFN-γ (dominant response)
• Tc2 → driven by IL-4

👉 Both kill, but differ in cytokines.

CYTOKINES

1️⃣ What are Cytokines? (Core Idea)

• Small protein messengers made by many cells: monocytes, macrophages, lymphocytes, endothelium, fibroblasts, epithelia.
• Main role: link innate and adaptive immunity.
• Act at very low concentrations via specific surface receptors.

Ways they act (must know):

• Autocrine – act on same cell that secreted it.
• Paracrine – act on nearby cells.
• Endocrine – act on distant cells via blood (less common, but possible).

2️⃣ Major Cytokine Groups & Key Examples

Just know functions + sources of the big ones.

A. Interferons (IFNs)

Job: early antiviral defence until adaptive immunity kicks in.

• IFN-α – from virally infected leukocytes
• IFN-β – from virally infected fibroblasts
• IFN-γ – from Th1 cells + NK cells

🔑 Functions of IFN-γ (very exam-high-yield):

1. Antiviral effects
2. ↑ MHC I + MHC II expression
3. Activates macrophages and NK cells
4. Makes target cells more susceptible to cytotoxic attack
5. Pushes Th0 → Th1 (Th1 polarisation)

B. Pro-inflammatory cytokines (the fire-starters)

Think of IL-1 and TNF-α as the first alarm signals of inflammation.

• IL-1
• Released mainly by macrophages and B cells
• Switches on immune cells like T cells, B cells, and NK cells
• Makes blood vessels express adhesion molecules, so white cells can stick and move into tissues
• TNF-α
• Released by macrophages and activated T cells
• Does almost the same job as IL-1
• Very important in the early response to infections, especially bacteria

👉 Bottom line:

When macrophages detect bacterial endotoxin (LPS) or cell stress, they release IL-1 and TNF-α to kick-start inflammation.

C.Chemokines (who-goes-where signals)

Chemokines are cytokines that act like GPS signals for immune cells.

• They pull cells toward a site by creating a chemical gradient
• Made by local tissue immune cells and endothelium
• Each immune cell has its own set of chemokine receptors, so only selected cells respond

Because of this:

• CCR5 mainly attracts Th1 cells
• CCR3 and CCR4 mainly attract Th2 cells

👉 Big picture:

Chemokines decide which type of T helper cell arrives, shaping the nature of the immune response at that site.

One-line exam lock

Chemokines don’t activate T cells — they decide which subtype shows up.

If you want, I can compress this into a single MCQ-safe sentence or a compare-with-IL-1/TNF-α block.

D. Growth factors (cell controllers)

Growth factors are signals that control blood cell formation and decide how cells mature and specialize.

• GM-CSF
• Released by macrophages, T cells, and fibroblasts
• Boosts the production of granulocytes and macrophages
• Also primes and activates these cells so they work better
• TGF-β
• Acts as an immune brake
• Slows down T- and B-cell proliferation
• Reduces activity of macrophages and natural killer (NK) cells

👉 Big picture:

GM-CSF pushes the immune response forward, while TGF-β keeps it under control.

3️⃣ MHC (HLA) – The Antigen Presentation System

T cells cannot see whole proteins.

They only respond to peptides presented on MHC molecules on APCs.

• Human MHC genes = HLA complex on chromosome 6p21.3
• Divided into:
• Class I
• Class II
• Class III

4️⃣ Class I MHC – “Show endogenous to CD8”

Types

• Classic: HLA-A, HLA-B, HLA-C
• On almost all nucleated cells
• Highly polymorphic (hundreds of alleles)
• Non-classic: HLA-E, HLA-F, HLA-G
• Limited polymorphism
• expressed only in specific tissues or cell types
• HLA-G → especially placenta (extravillous cytotrophoblast)

Function

• Present 8–9 amino acid peptides from inside the cell (endogenous antigens – e.g. viruses)
• Present to CD8⁺ cytotoxic T cells
• Allows Tc cells to kill infected cells and clear intracellular pathogens.

👉 One-liner:

Class I = all nucleated cells, endogenous peptides, CD8.

5️⃣ Class II MHC – “Show exogenous to CD4”

• Encodes HLA-DR, HLA-DQ, HLA-DP
• Expressed on professional APCs:
• Monocytes/macrophages
• B cells
• Dendritic cells

Function

• Groove is open-ended → binds longer peptides (15–24 aa)
• Presents exogenous peptides (taken up from outside the cell)
• Presents to CD4⁺ T helper cells

👉 One-liner:

Class II = APCs, exogenous peptides, CD4.

6️⃣ Class III MHC – “Support proteins nearby”

• Not peptide-presenting.
• Region contains genes for:
• Complement components: C2, C4, factor B
• Heat shock proteins: HSP70 family
• TNF-α

👉 Think: soluble defence proteins, not antigen presenters.

🧬 CYTOKINES & MHC — COMPLETE COMPARATIVE TABLES (ZERO-OMISSION)

TABLE 1️⃣ — What Are Cytokines? (Core Definition & Action Modes)

TABLE 2️⃣ — Major Cytokine Groups (Overview)

TABLE 3️⃣ — Interferons (IFNs)

TABLE 4️⃣ — Pro-Inflammatory Cytokines (Early Alarm Signals)

Trigger for release:

Macrophage detection of bacterial endotoxin (LPS) or cell stress

TABLE 5️⃣ — Chemokines (Cell-Migration Controllers)

TABLE 6️⃣ — Growth Factors

Big picture:

GM-CSF accelerates immunity — TGF-β restrains it

🧫 MHC (HLA) SYSTEM TABLES

TABLE 7️⃣ — MHC Overview

TABLE 8️⃣ — Class I MHC (“Endogenous → CD8”)

Exam one-liner:

Class I = all nucleated cells, endogenous peptides, CD8

TABLE 9️⃣ — Class II MHC (“Exogenous → CD4”)

Exam one-liner:

Class II = APCs, exogenous peptides, CD4

TABLE 🔟 — Class III MHC

FINAL EXAM LOCK (Ultra-Short)

Cytokines signal, chemokines direct traffic, MHC shows peptides — CD8 kills, CD4 coordinates.

🚀 TRANSPLANTATION

Transplant success depends on donor–recipient compatibility, especially HLA (MHC).

1️⃣ Types of Grafts – MUST KNOW

👉 Exam focus:

Allografts and xenografts activate recipient T cells → rejection.

2️⃣ Allorecognition – WHY grafts get rejected

Two key reasons:

A. Passenger Dendritic Cells (Super High Yield)

• Donor dendritic cells carry donor MHC.
• They migrate out of graft → activate naïve recipient T cells.
• They are professional APCs, so the response is very strong.

B. High frequency of T cells reacting to foreign MHC

• Many recipient T cells can recognise allogeneic MHC even without peptide match.
• → Makes rejection response much stronger than against infections.

Minor Histocompatibility Antigens

• Even if MHC is identical → minor antigens can cause rejection.
• Most important: H-Y antigen (on Y chromosome) → male cells only.

3️⃣ Graft-versus-Host Disease (GVHD) – Opposite of rejection

Occurs mainly in bone marrow transplantation.

• Immune-competent donor T cells attack recipient tissues.
• Trigger against recipient MHC or minor antigens.

Prevention:

• HLA matching
• Removal of donor T cells
• Immunosuppression

👉 Exam tip:

“Rejection = host attacks graft.

GVHD = graft attacks host.”

4️⃣ Types of Rejection – The Core Exam Topic

➡️ 1. Hyperacute Rejection

Time: minutes–hours

Cause: Preformed antibodies (IgG) in recipient against donor antigens

• ABO incompatibility
• Anti-donor MHC due to previous transplant, pregnancy, transfusion

Mechanism:

Antibody binding → complement activation, thrombosis, vascular leak → graft death

👉 Immediate and irreversible.

➡️ 2. Acute Rejection

Time: days–weeks

Cause: Primary immune response

Mechanism:

• Donor “passenger leukocytes” leave graft → activate host T cells
• Host CD4⁺ (Th1) → delayed hypersensitivity
• Host CD8⁺ (Tc) → kill donor cells

👉 Reversible with immunosuppression.

➡️ 3. Chronic Rejection

Time: months–years

Mechanism:

• Progressive vascular narrowing, fibrosis
• Macrophage infiltration
• Smooth muscle proliferation
• Ischemia of graft

👉 Slowly progressive → major cause of long-term graft failure.

5️⃣ Preventing Rejection – The Only Two Ways

1. HLA Matching

• Best possible match → better graft survival
• Class II mismatches cause more severe rejection than class I
• A single class II mismatch ≈ as bad as 3–4 class I mismatches

👉 If both class I and II mismatched → very rapid rejection.

2. Immunosuppressive Drugs (Table 19.5 High Yield)

👉 Most important: Ciclosporin & Tacrolimus → T cell activation blocked.

🚀 HYPERSENSITIVITY

Hypersensitivity = harmful, exaggerated immune response → tissue damage.

There are 4 types.

Each type is defined by mechanism, immune component, and examples.

If you remember the mechanism + examples, you will ace any exam question.

1️⃣ TYPE I – Immediate (IgE-mediated)

Mechanism:

• Allergen enters via inhalation/ingestion
• Binds IgE already attached to mast cells/basophils
• Cross-linking → mast cell degranulation
• Releases histamine → vasodilation, bronchoconstriction → allergy symptoms
• INCREASE TRIPTASE

Timing: seconds to minutes

Examples:

• Anaphylaxis (peanuts, bee venom, penicillin)
• Asthma
• Hay fever
• Urticaria (weal and flare reaction)

👉 Key idea: IgE + mast cells → histamine → immediate reaction.

2️⃣ TYPE II – Antibody-mediated (IgG/IgM)

Mechanism:

• IgG or IgM bind to antigens on host cells
• Antibodies recruit:
• Complement
• Neutrophils
• Platelets
• → cell destruction + inflammation

Timing: minutes to hours

Examples:

• Transfusion reactions (wrong blood group)
• Haemolytic disease of the newborn (Rh incompatibility)
• Certain drug-induced haemolysis
• hashimotos thyroiditis
• rheumatic fever

👉 Key idea: Antibody targets cells → destruction.

3️⃣ TYPE III – Immune Complex–mediated

Mechanism:

• Failure to clear antigen–antibody complexes
• Complexes deposit in tissues (vessels, joints, kidneys)
• Activate complement → recruit neutrophils
• Neutrophils release enzymes → tissue damage

Examples:

• Autoimmune diseases:
• SLE
• Rheumatoid arthritis
• Chronic infections:
• Leprosy
• Viral hepatitis
• Hypersensitivity pneumonitis:
• Farmer’s lung
• Pigeon fancier’s lung
• Serum sickness

👉 Key idea: Immune complexes stick to tissues → complement → inflammation.

4️⃣ TYPE IV – Delayed (T-cell mediated)

Mechanism:

• Sensitised T cells (CD4 or CD8) respond to antigen at site
• Reaction develops over 24–72 hours
• No antibodies involved
• 3 forms:

A. Contact dermatitis

• Nickel, chromate
• Eczema-like rash at site

B. Tuberculin-type reaction

• PPD test (Mantoux)
• Local swelling from memory T cells

C. Granulomatous type

• Persistent antigen → chronic T-cell activation
• Cytokines (TNF-α) → granuloma formation
• Seen in:
• TB
• Leprosy
• Crohn’s disease

👉 Key idea: T-cells cause inflammation → delayed onset.

🧠 HYPERSENSITIVITY — COMPLETE MASTER TABLE (ZERO OMISSION)

📌 CLASSIC EXAMPLES (HIGH-YIELD)

🧠 EXAM LOCK — ONE-LINE MEMORY KEYS

• Type I: IgE + mast cell + histamine → immediate allergy
• Type II: Antibody attacks host cell
• Type III: Immune complexes deposit in tissues
• Type IV: T-cells only → delayed reaction

⚠️ COMMON EXAM TRAPS (DON’T MISS)

• Mantoux test = Type IV (NOT antibody-mediated)
• SLE = Type III (immune complexes, NOT Type II)
• Anaphylaxis = Type I (IgE)
• Granuloma formation = Type IV
• Complement activation = Types II & III only

fetus as an allograft

1️⃣ Core Idea: Why Doesn’t the Mother Reject the Fetus?

• Fetus is half paternal → immunologically like a semi-allograft.
• But normally not rejected → because:
• The placenta is the real interface, not the fetus directly.
• The placenta is designed immunologically to avoid classic graft rejection and to actively promote tolerance.

2️⃣ Two Maternal–Fetal Interfaces (Only the Essence)

Interface 1 – Tissue–Tissue (Decidua ↔ Extravillous Cytotrophoblast)

• Extravillous cytotrophoblast:
• Invades decidua + spiral arteries → remodels them → ↑ blood flow.
• Decidua immune cells ≈ 40% of cells:
• Majority = special NK cells (decidual NK, CD56⁺ bright, no CD16⁻)
• Some T cells, macrophages, dendritic cells
• Virtually no B cells

👉 These NK cells are not killers here – they mainly secrete cytokines, chemokines, angiogenic factors that help trophoblast invasion and placentation.

Interface 2 – Tissue–Blood (Syncytiotrophoblast ↔ Maternal Blood)

• Syncytiotrophoblast lines villi and is bathed in maternal blood.
• In contact with all maternal blood cells.
• Sheds:
• Microparticles, DNA, mRNA into maternal blood
• Occasional fetal RBCs and leukocytes → can reach maternal circulation (basis for immunisation, Rh disease).

3️⃣ Crucial MHC Pattern on Trophoblast (EXAM GOLD)

Extravillous Cytotrophoblast (Interface 1)

• Class I positive but with a very special pattern:
• Does NOT express: HLA-A, HLA-B (highly polymorphic, main graft rejection drivers)
• DOES express:
• Classic: HLA-C (polymorphic)
• Non-classic: HLA-E, HLA-G (low polymorphism)

Syncytiotrophoblast (Interface 2)

• No class I MHC at all (almost unique, like RBCs).
• No class II either.
• So it doesn’t present antigen to maternal T cells → unlikely to trigger classic T cell–mediated rejection.

Class II

• Neither trophoblast type expresses class II → again reduces T cell activation.

👉 Key exam line:

Placenta avoids classic T-cell rejection by:

• Not expressing HLA-A/B or class II
• Using HLA-C, -E, -G mainly to signal to NK cells, not T cells.

4️⃣ HLA-G, HLA-E, HLA-C – What You Actually Have to Know

HLA-G (Super High Yield)

• On extravillous cytotrophoblast.
• Low polymorphism → paternal HLA-G ≈ maternal HLA-G → less likely to activate alloreactive T cells.
• Has membrane forms (e.g. HLA-G1) and soluble forms (e.g. HLA-G5).

Functions:

• Can bind peptides, but probably mainly for molecule stability, not broad antigen presentation.
• Acts on CD4⁺ and CD8⁺ T cells:
• Induces apoptosis of CD8⁺ T cells (via Fas–FasL)
• Suppresses CD4⁺ T-cell and Tc proliferation
• Binds NK and myeloid receptors:
• KIR2DL4, ILT-2, ILT-4 on NK cells, monocytes, macrophages, dendritic cells
• Result = not attack, but support implantation:
• Decidual NK cells produce:
• Cytokines: IFN-γ, IL-10, TGF-β1
• Chemokines: IL-8, IP-10
• Angiogenic factors: VEGF, PlGF(placental growthfactor)

→ Enhance trophoblast invasion + vascular remodelling

HLA-E

• Also on extravillous trophoblast and many other cells.
• Low polymorphism.
• Binds peptides from leader sequences of other class I molecules (HLA-A/B/C/G).
• Interacts with NK receptors → contributes to NK modulation, not classic T-cell-driven rejection.

HLA-C

• Polymorphic, in theory could provoke T-cell rejection.
• But here the main interaction is again with NK cells, via KIRs.
• NK–HLA-C cross-talk controls cytokine and angiogenic factor production.

👉 Key clinical point:

Specific HLA-C / KIR combinations can promote or inhibit invasion:

• HLA-C1 + activating KIR-B on NK → good invasion → normal placentation
• HLA-C2 + inhibitory KIR-A → poor NK activation → shallow invasion → pre-eclampsia/recurrent miscarriage association

5️⃣ Maternal Antibody Responses – Why They Usually Don’t Harm the Fetus

• Fetal leukocytes (with HLA-A, -B, -C) can enter maternal blood.
• Mother can form antibodies to paternal HLA:
• About 15% of first pregnancies
• About 60% of later pregnancies with same father
• These antibodies usually don’t harm the fetus because:

Placental “Filter” Mechanism:

• Only IgG crosses the placenta (via Fc receptors on syncytiotrophoblast).
• Potentially harmful anti-paternal HLA antibodies:
• cross syncytiotrophoblast
• but then bind to HLA on villus macrophages/endothelium
• form immune complexes, which are:
• cleared by villous macrophages
• protected from complement by regulatory proteins (e.g. decay-accelerating factor)

→ So they don’t reach fetal circulation in destructive form.

Exception: Haemolytic Disease of the Newborn (RhD)

• Here mother makes IgG against fetal RBC antigen (RhD).
• IgG crosses placenta → binds fetal RBCs → haemolysis.
• Typically:
• First RhD⁺ baby of RhD⁻ mother usually okay
• Sensitisation at delivery → memory B cells
• Subsequent RhD⁺ babies → hemolysis, anaemia, liver/spleen dysfunction, can be fatal.
• Prevention: Anti-D prophylaxis postpartum:
• Inject anti-RhD IgG → coat fetal RBCs in mum’s blood → clear them before she becomes sensitised.

6️⃣ Th1/Th2 Shift in Pregnancy – KEY CONCEPT

• Normal pregnancy = bias towards Th2 (antibody) and away from Th1 (cell-mediated) responses.

Mechanism:

• Placenta produces:
• IL-4, IL-10 → Th2-promoting cytokines
• Progesterone → inhibits Th1, including IFN-γ production.

Effect:

• Cell-mediated (Th1) responses suppressed
• Humoral (Th2) responses preserved → infection defence via antibodies maintained.

Clinical evidence:

• Rheumatoid arthritis (Th1-mediated) → often improves in pregnancy.
• Diseases with intracellular pathogens (e.g. herpes, malaria) → worsen (need Th1).
• SLE (Th2-driven autoantibody disease) → often worsens in pregnancy.

7️⃣ When Things Go Wrong – Immune Mechanisms in Pregnancy Disorders

A. Abnormal HLA-G / HLA-C Patterns

• ↓ HLA-G on extravillous trophoblast → linked to recurrent miscarriage, pre-eclampsia.
• HLA-C2 + inhibitory KIR-A combinations → poor trophoblast invasion → more common in pre-eclampsia, recurrent miscarriage.

B. Th1/Inflammatory Shift in Pathology

• In pre-eclampsia/recurrent miscarriage:
• Higher IFN-γ and inflammatory markers (e.g. CRP)
• Stronger systemic inflammatory response
• Leads to endothelial dysfunction: hypertension, proteinuria, oedema, DIC.

C. Antiphospholipid Antibodies

• Lupus anticoagulant and anticardiolipin antibodies → ↑ miscarriage risk.
• Interfere with:
• Coagulation (prothrombin → thrombin)
• Trophoblast maturation + placentation
• Treatment: Low-dose aspirin ± heparin can improve outcomes.
• They can cross placenta → transient neonatal autoimmune issues.

FETUS AS AN ALLOGRAFT — COMPLETE INTEGRATED TABLE (ZERO OMISSION)

One-Line Exam Reflex (Lock It):

The fetus survives as a semi-allograft because the placenta avoids classical T-cell recognition (no HLA-A/B or class II), actively modulates NK cells via HLA-C/E/G, biases immunity toward Th2, and filters maternal antibodies.