The Immune Response to Infection: A Stepwise Overview

Innate Immunity (Hours 0–96)

1. Recognition: PAMPs (LPS, flagellin, dsRNA) bind PRRs (TLRs, NLRs, RLRs) on macrophages, dendritic cells.
2. Inflammation: Cytokines (TNF, IL-1, IL-6), chemokines → vasodilation, endothelial activation, leukocyte recruitment.
3. Phagocytosis: Neutrophils (first), macrophages engulf pathogens; oxidative burst, NETs.
4. Complement: Opsonization (C3b), chemotaxis (C5a), MAC lysis.
5. NK cells: Kill virus-infected/tumor cells (missing MHC-I).

Bridge to Adaptive Immunity

• Dendritic cells migrate to lymph nodes, present antigen (MHC-II) to naïve CD4+ T cells.
• Co-stimulation (CD28/B7) + cytokines → T-cell priming.

Adaptive Immunity (Days 4–7+)

1. Th1: IFN-γ → macrophage activation, IgG opsonization (intracellular pathogens).
2. Th2: IL-4/5/13 → IgE, eosinophils (helminths, allergy).
3. Th17: IL-17 → neutrophil recruitment (extracellular bacteria/fungi).
4. Tfh: B-cell help → germinal centers, affinity maturation, class switching.
5. CTLs (CD8+): Kill infected cells via perforin/granzyme, FasL.
6. Antibodies: Neutralize, opsonize, activate complement, ADCC.

Resolution and Memory

• Regulatory T cells (Treg), IL-10, TGF-β, resolvins dampen inflammation.
• Memory T/B cells persist → faster, stronger secondary response.

Variability

Pathogen type, host genetics, age, microbiome, comorbidities shape response magnitude and quality.