• Immune Architecture of the Spleen: The spleen is the largest secondary lymphoid organ in the body and functions as a specialized 'lymph node for the blood'.
• Filtering Mechanism: While conventional lymph nodes possess afferent lymphatic vessels that filter interstitial tissue lymph, the spleen receives arterial blood directly via the splenic artery. In the marginal zone and white pulp (periarteriolar lymphoid sheaths, PALS, and follicular B-cell zones), specialized macrophages and dendritic cells capture, process, and present blood-borne antigens, initiating systemic humoral and cell-mediated immune responses.

Correct option: (2) Spleen

• Role of Decay-Accelerating Factor (CD55): CD55 (Decay-Accelerating Factor, DAF) is a 70-kDa glycosylphosphatidylinositol (GPI)-anchored cell surface regulatory glycoprotein that protects normal host autologous cells from accidental complement-mediated lysis.
• Mechanism: CD55 binds to membrane-bound C3 convertases of both the classical/lectin pathway ($C4b2a$) and alternative pathway ($C3bBb$), accelerating their rapid dissociation and preventing formation of the terminal membrane attack complex (MAC).
• Contrasting Complement Regulators:
• CD59 (Protectin / MAC-IP): Binds directly to C8 and C9, blocking polymerisation of the MAC pore.
• CD21 (CR2): Complement receptor 2 on B cells that binds C3d.
• CD23: Low-affinity receptor for IgE (Fc$\epsilon$RII).

Correct option: (1) CD55

• Adrenergic Regulation of Mast Cell Degranulation: Epinephrine (adrenaline) is the drug of choice for acute anaphylactic shock. Beyond inducing vascular constriction and bronchodilation, it directly binds to $\beta_2$-adrenoceptors on the surface of tissue mast cells and basophils.
• Biochemical Cascade: $\beta_2$-adrenoceptor stimulation activates membrane-bound adenylate cyclase via $G_s$, raising intracellular cyclic adenosine monophosphate (cAMP) levels. Elevated cAMP blocks intracellular calcium mobilization ($Ca^{2+}$ influx), powerfully inhibiting mast cell degranulation and the release of histamine, leukotrienes, and PAF.
• Contrasting Drugs:
• Propranolol: Non-selective $\beta$-blocker (prevents inhibition, exacerbates degranulation).
• Phenylephrine: Selective $\alpha_1$-agonist.

Correct option: (4) Epinephrine

• Mouse Major Histocompatibility Complex (H-2): In laboratory mice (Mus musculus), the Major Histocompatibility Complex is designated H-2 (Histocompatibility-2).
• Historical Context: In the 1930s, George Snell and Peter Gorer identified cell-surface alloantigens responsible for the rapid rejection of grafted tumors and skin transplants, naming the locus Histocompatibility locus 2 (H-2) on chromosome 17 decades before its fundamental role in physiological T-cell antigen presentation was discovered.
• Species Nomenclature Breakdown:
• Mouse: H-2
• Human: HLA (Human Leukocyte Antigen)
• Cattle: BoLA (Bovine Leukocyte Antigen)
• Dog: DLA (Dog Leukocyte Antigen)
• Horse: ELA (Equine Leukocyte Antigen)

Correct option: (3) H-2