for everything i am gonna paste can u give me correc answer and also explain in simple terms why
All of the following can cause congenital infection or infections of the newborn EXCEPT A) Syphilis B) Gonorrhea C) nongonococcal urethritis D) genital herpes E) lymphogranuloma vanereum
| STI | Causes Newborn Infection? | How? |
|---|---|---|
| A) Syphilis | YES | Crosses the placenta - classic congenital infection causing stillbirth, bone/skin/organ damage in baby |
| B) Gonorrhea | YES | Baby's eyes get infected during vaginal birth (ophthalmia neonatorum - can cause blindness) |
| C) Nongonococcal urethritis (Chlamydia) | YES | Chlamydia is the main cause - infects baby's eyes and lungs during delivery |
| D) Genital Herpes (HSV) | YES | Baby gets infected passing through the birth canal - can cause severe brain/skin/organ disease |
| E) LGV | NO | LGV is caused by Chlamydia trachomatis serovars L1-L3. It causes lymph node swelling (buboes) in adults, but is NOT known to cause congenital or neonatal infection |
T cells are made in the_____ A. Bone marrow B. Spleen C. Thymus D.Tonsils E MALT
| Option | Role in Immune System | Why NOT the answer |
|---|---|---|
| A) Bone Marrow | Makes ALL blood cell precursors + matures B cells | T cells are only born here, not made/matured |
| B) Spleen | Filters blood, activates immune responses | Secondary lymphoid organ - not where T cells are made |
| D) Tonsils | First line of defense in throat | Secondary lymphoid tissue - not a T cell factory |
| E) MALT | Gut/airway immune defense | Secondary lymphoid tissue - not where T cells mature |
T cell = Thymus (same first letter!) B cell = Bone marrow (same first letter!)
Nongonococcal urethritis can be caused by all of the following EXCEPT A. Mycoplasma homini. B. Candida albicans. C. Trichomonas vaginalis. D. streptococci. E. Neisseria gonorrhoeae
| Organism | Causes NGU? | Notes |
|---|---|---|
| A) Mycoplasma hominis | ✅ YES | Mycoplasma/Ureaplasma species are recognized NGU causes, accounting for many cases |
| B) Candida albicans | ✅ YES | Fungal infection can cause urethral inflammation (urethritis) - though less common |
| C) Trichomonas vaginalis | ✅ YES | A parasitic protozoan - well-known cause of NGU |
| D) Streptococci | ✅ YES | Bacterial cause of urethritis that falls under the NGU umbrella |
| E) N. gonorrhoeae | ❌ NO | This causes gonococcal urethritis - the opposite category! |
Source: Robbins Pathologic Basis of Disease - "Nongonococcal urethritis is common and can be caused by several different organisms. Various strains of Chlamydia are the cause of 25-60% of nongonococcal urethritis in males."
74.Large size antibodies that agglutinate antigens are A) Ig G B) Ig M C) Ig E D) Ig A E) Ig
Normal IgG = Y shape → 2 binding sites
IgM = 5 Y's joined together → 10 binding sites
| Antibody | Size | Key Role | Why NOT the answer |
|---|---|---|---|
| A) IgG | Medium (monomer) | Main antibody in blood, crosses placenta | Smaller, only 2 binding sites |
| C) IgE | Small (monomer) | Allergies and parasites | Tiny amount in blood, not an agglutinator |
| D) IgA | Medium (dimer) | Found in saliva, tears, breast milk | 4 binding sites, but not the best agglutinator |
| E) IgD | Small (monomer) | B cell activation signal | Barely present in blood, no agglutination role |
| Feature | Detail |
|---|---|
| Structure | Pentamer (5 units) |
| Binding sites | 10 (most of any antibody) |
| Size | Largest antibody (~900 kDa) |
| First responder | First antibody made during any new infection |
| Best at | Agglutination & complement activation |
IgM = Massive, Multiple, first iMmune response
- Massive size
- Multiple binding sites (10!)
- First antibody made (M = first response)
12 B. Pinocytosis C. Exocytosis D. Endocytosis 73. The specificity of an antibody is due to A) Its valence B) The H chains C) The L chains. D) The constant portions of the H and L chains. E) The variable portions of the H and L chains 74.Large size antibodies that agglutinate antigens are A) Ig G B) Ig M C) Ig E D) Ig A E) Ig 75.Antigens can be A) Proteins B) Polysaccharides C) Lipids D) Nucleic acids E) All of these
Antigen binds HERE
↓
[Variable H + Variable L] ← SPECIFICITY lives here
[Constant H + Constant L] ← same in all IgG, for example
| Option | Why Wrong |
|---|---|
| A) Valence | Valence = number of binding sites (2 in IgG), not specificity |
| B) H chains alone | Both H AND L variable regions together determine specificity |
| C) L chains alone | Same - you need both H and L variable portions |
| D) Constant portions | Constant regions determine antibody CLASS (IgG, IgM etc.), not specificity |
Memory trick: Variable = Varies per antigen = determines specificity
| Type | Example | Antigen? |
|---|---|---|
| A) Proteins | Bacterial surface proteins, viral coat proteins | ✅ YES - most common antigens |
| B) Polysaccharides | Bacterial capsules (e.g. pneumococcus), ABO blood group antigens | ✅ YES |
| C) Lipids | Lipid A of LPS, mycobacterial lipids | ✅ YES - especially with carrier proteins |
| D) Nucleic acids | DNA antigens in autoimmune disease (e.g. anti-dsDNA in lupus) | ✅ YES |
Any molecule that is foreign to the body and large enough (or attached to a carrier) can act as an antigen. The immune system doesn't care what chemical class it belongs to!
| Q | Answer | Key Concept |
|---|---|---|
| 73 | E - Variable portions of H & L chains | Variable regions = specificity |
| 74 | B - IgM | Pentamer, largest, best agglutinator |
| 75 | E - All of these | Antigens can be any biomolecule |
76.An antibody has a) 2 Fab regions and an Fc region b) an Fab region and an Fc region c) 2 Fab regions and 2 Fc regions d) many Fab regions and many Fc regions
[Fab] [Fab]
\ /
\ / ← The 2 arms of the Y
\ /
[Fc] ← The stem/tail of the Y
| Region | Full Name | What it Does |
|---|---|---|
| Fab | Fragment antigen binding | Grabs and binds to the antigen (the "hands") |
| Fc | Fragment crystallizable | Binds to immune cell receptors, activates complement (the "signal tail") |
| Option | Why Wrong |
|---|---|
| B) 1 Fab + 1 Fc | Missing one Fab - there are always 2 arms on the Y |
| C) 2 Fab + 2 Fc | There is only ever ONE Fc (one stem on the Y) |
| D) Many Fab + many Fc | That would describe IgM (pentamer), but even then it has 10 Fab + 5 Fc - not the standard answer for a basic antibody |
Think of the Y shape:
- 2 arms = 2 Fab (two hands to grab antigens)
- 1 stem = 1 Fc (one tail to signal immune system)
80.The different lineage of the lymphocytes can be distinguished by characterizing the expression of their membrane molecules called the cluster of differentiation (CD). Which of the following CD is only found in B-cells? A) CD4 B) CD8 C) CD40 D) CD 19, 20
| CD Marker | Found On | B Cell Only? |
|---|---|---|
| A) CD4 | Helper T cells (and some macrophages/dendritic cells) | ❌ NO - T cell marker |
| B) CD8 | Cytotoxic T cells | ❌ NO - T cell marker |
| C) CD40 | B cells, dendritic cells, macrophages, endothelial cells | ❌ NO - found on multiple cell types |
| D) CD19, CD20 | B cells ONLY | ✅ YES - exclusive B cell markers |
B CELLS: CD19, CD20, CD21, CD22 ← B cell exclusive
Helper T: CD4 ← T cell marker
Cytotoxic T: CD8 ← T cell marker
All T cells: CD3 ← Pan-T cell marker
NK cells: CD16, CD56
Rituximab is a monoclonal antibody drug that targets CD20 on B cells. It is used to treat:
- B cell lymphomas
- Rheumatoid arthritis
- Multiple sclerosis
This works because CD20 is ONLY on B cells - so the drug selectively destroys B cells without harming other immune cells!
B cells = CD19, 20 → think "B comes before T in the alphabet, and 19-20 are the teen numbers" T helper = CD4 → "4 = helper" (4 letters in "help") T killer = CD8 → "8 = kill" (8 looks like two bullets)
79.Which of the following immune cells are not derived from lymphoid progenitor cells? A. T cells B. B cells C. Natural killer (NK) cells D. Neutrophils
Hematopoietic Stem Cell (HSC)
|
_____|_____
| |
LYMPHOID MYELOID
progenitor progenitor
| |
| Neutrophils ← HERE
T cells Monocytes
B cells Eosinophils
NK cells Basophils
Red blood cells
Platelets
| Cell | Progenitor | Derived from Lymphoid? |
|---|---|---|
| A) T cells | Lymphoid progenitor → Thymus | ✅ YES - classic lymphocyte |
| B) B cells | Lymphoid progenitor → Bone marrow | ✅ YES - classic lymphocyte |
| C) NK cells | Lymphoid progenitor | ✅ YES - part of lymphoid family |
| D) Neutrophils | Myeloid progenitor | ❌ NO - myeloid cell, not lymphoid |
Neutrophils = "N" for Not lymphoid The classic lymphocytes are T, B, and NK - anything else (neutrophils, macrophages, eosinophils) is myeloid
82.Immunogens are the antigens that can evoke an immune response. Which of the following is not an immunogen? a) Protein b) Lipopolysaccharides c) Polysaccharides d) Hapten
HAPTEN alone:
✅ Can bind to antibodies (it IS an antigen)
❌ Cannot trigger immune response alone (NOT an immunogen)
HAPTEN + Carrier Protein:
✅ NOW it can trigger a full immune response
✅ Becomes an immunogen
| Substance | Immunogen? | Why |
|---|---|---|
| A) Protein | ✅ YES | Large, complex molecules - best immunogens. Most vaccines use proteins |
| B) Lipopolysaccharides (LPS) | ✅ YES | Large molecules on bacterial surfaces - strong immune stimulators |
| C) Polysaccharides | ✅ YES | Large enough to trigger immune response (e.g. pneumococcal vaccine) |
| D) Hapten | ❌ NO | Too small to trigger immune response alone - needs carrier protein |
| Hapten | Carrier | Clinical Significance |
|---|---|---|
| Penicillin | Serum proteins | Causes penicillin allergy reactions |
| Urushiol (poison ivy) | Skin proteins | Causes contact dermatitis |
| Drugs (sulfa drugs) | Body proteins | Drug hypersensitivity reactions |
| Dinitrophenol (DNP) | BSA (in lab) | Classic experimental hapten |
ANTIGEN: Can be RECOGNIZED by immune system
IMMUNOGEN: Can TRIGGER immune response by itself
All immunogens are antigens
BUT not all antigens are immunogens ← HAPTEN is the perfect example!
Hapten = "Half-antigen" (the word comes from Greek "haptein" = to fasten) It can fasten/bind to an antibody, but it's only half the story - it needs a carrier to be a full immunogen!
83.The hybridomas are made by : A) fusinf T cells with myloma cells B) fusing B cells with myeloma cells C) fusing T helper cells with with myeloma cells D) fusing B memory cells with myeloma cells
B cell + Myeloma cell
(makes antibodies) (lives forever)
↓ FUSION ↓
HYBRIDOMA
(makes antibodies AND lives forever!)
| Option | Why Wrong |
|---|---|
| A) T cells + myeloma | T cells do NOT make antibodies - wrong cell type entirely |
| B) B cells + myeloma | ✅ CORRECT - B cells are the antibody producers |
| C) T helper cells + myeloma | T helper cells coordinate immune response but do NOT make antibodies |
| D) B memory cells + myeloma | Close but incomplete - it is specifically activated B cells (plasma cells/splenocytes) used, not memory B cells specifically. The standard answer is simply "B cells" |
Step 1: Inject mouse with antigen
↓
Step 2: Mouse makes B cells that produce antibody against that antigen
↓
Step 3: Remove spleen (full of B cells) from mouse
↓
Step 4: FUSE B cells with myeloma cells using PEG (polyethylene glycol)
↓
Step 5: HYBRIDOMA formed
↓
Step 6: Grow in HAT medium (kills unfused cells)
↓
Step 7: Select the hybridoma making the RIGHT antibody
↓
Step 8: Clone it → produces MONOCLONAL ANTIBODIES forever!
| Drug | Target | Used For |
|---|---|---|
| Rituximab | CD20 on B cells | Lymphoma, RA |
| Herceptin | HER2 receptor | Breast cancer |
| Infliximab | TNF-alpha | Crohn's, RA |
| Adalimumab | TNF-alpha | Autoimmune diseases |
Hybridoma = Hybrid of antibody-making cell + immortal cancer cell B cell makes antibodies → B is for Bodies (antibodies) Myeloma = immortal → never dies in culture Together = immortal antibody factory!
88.What type of cells are generally found in lower concentration in autoimmune disease? A) T cells B) B cells C) Treg D) Macrophages E) CTL
Normal Immune System:
Self-antigen appears
↓
Immune cells start to react
↓
TREG says "STOP! That's our own tissue!"
↓
Immune response is SUPPRESSED ✅ = No autoimmunity
Autoimmune Disease:
Self-antigen appears
↓
Immune cells start to react
↓
TREG is LOW/ABSENT ← the problem!
↓
Immune response is NOT suppressed ❌ = Attacks own tissues!
| Cell | In Autoimmune Disease | Why NOT the answer |
|---|---|---|
| A) T cells | Usually INCREASED | T cells are the attackers in autoimmunity |
| B) B cells | Usually INCREASED | B cells make autoantibodies (e.g. anti-dsDNA in lupus) |
| C) Treg | ✅ DECREASED | The "brake" on immune system is lost |
| D) Macrophages | Usually INCREASED | Drive inflammation in autoimmune diseases |
| E) CTL (Cytotoxic T cells) | Usually INCREASED | These are the tissue-destroying cells in autoimmunity |
| Disease | What Tregs Fail to Suppress |
|---|---|
| Type 1 Diabetes | Attack on pancreatic beta cells |
| Multiple Sclerosis | Attack on myelin in brain/spinal cord |
| Rheumatoid Arthritis | Attack on joint synovium |
| Systemic Lupus (SLE) | Attack on DNA, kidneys, skin |
| IPEX Syndrome | Severe Treg deficiency from birth - causes massive multi-organ autoimmunity |
- CD4⁺ CD25⁺ FoxP3⁺ = the classic Treg cell signature
- FoxP3 is the master transcription factor for Tregs
- Tregs work by releasing IL-10 and TGF-β (anti-inflammatory cytokines)
Treg = Traffic Regulation for the immune system No traffic cop (Treg) = cars (immune cells) crash into everything (your own organs) Low Treg = Autoimmunity chaos!