# Situation: A 26-year-old woman with systemic lupus erythematosus (SLE) comes to the medical outpatient clinic for follow-up. She takes hydroxychloroquine daily and prednisone 5 mg daily. Her usual blood pressure is 110/70 mmHg. Which type of hypersensitivity reaction causes the tissue damage in SLE?

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> subject: Nursing Practice III — Care of Clients with Problems in Surgery, Oxygenation, Fluid and Electrolytes, Infectious, Inflammatory and Immunologic Response, Cellular Aberrations

## 문제

Situation: A 26-year-old woman with systemic lupus erythematosus (SLE) comes to the medical outpatient clinic for follow-up. She takes hydroxychloroquine daily and prednisone 5 mg daily. Her usual blood pressure is 110/70 mmHg.

Which type of hypersensitivity reaction causes the tissue damage in SLE?

## 보기

1. Type III, immune complex deposition **✔ 정답**
2. Type II, cytotoxic (antibody against cell surfaces)
3. Type I, immediate (immunoglobulin E–mediated)
4. Type IV, delayed (T cell–mediated)

**정답: 1**

## 해설

In SLE, antigen–antibody (immune) complexes deposit in vessels, kidneys, joints, and skin and trigger inflammation, which is a type III reaction. Serum sickness and post-streptococcal glomerulonephritis are other type III examples. Type II reactions, such as myasthenia gravis, involve antibodies directed at cell surface receptors.

## 심화 해설

Core mechanism

Systemic lupus erythematosus is the classic example of a type III hypersensitivity reaction. The tissue injury begins when autoantibodies bind circulating self-antigens—especially nuclear material such as double-stranded DNA and nucleosomes—to form soluble antigen–antibody immune complexes. Because these complexes are small and soluble, they are not cleared efficiently. They deposit in vascular walls, renal glomeruli, joints, and skin, where they activate complement and attract neutrophils. The resulting inflammation and enzymatic damage produce the multisystem findings of SLE [1].

Immune complex deposition, not direct antibody attack on a fixed cell surface, is the central driver of organ damage in SLE. This is why the disease can involve so many different tissues at the same time.

| Hypersensitivity type | Key effector | Clinical example | SLE relevance |
| --- | --- | --- | --- |
| Type I | IgE, mast cells, histamine | Anaphylaxis, allergic rhinitis | Not the mechanism of SLE tissue damage |
| Type II | IgG or IgM against cell surface or matrix antigens | Myasthenia gravis, autoimmune hemolytic anemia | Autoantibodies exist, but organ damage is not primarily from direct cytotoxicity |
| Type III | Soluble immune complexes, complement, neutrophils | SLE, serum sickness, post-streptococcal glomerulonephritis | Primary mechanism of tissue injury |
| Type IV | Sensitized T cells, macrophages | Contact dermatitis, tuberculin reaction | Not the principal pathway in SLE |

Watch out! SLE patients do produce autoantibodies such as anti-dsDNA and antinuclear antibodies, which can tempt a choice of type II. However, the presence of autoantibodies alone does not define type II. In type II, the antibody binds directly to a fixed cell surface or tissue antigen and causes damage at that site. In SLE, the antibodies bind soluble nuclear antigens, and the resulting immune complexes travel and deposit elsewhere—that is type III [1].

The distinction between type II and type III depends on whether the antibody attacks a fixed tissue antigen directly or forms a circulating complex that deposits secondarily. Myasthenia gravis illustrates type II because antibodies target acetylcholine receptors on the motor end plate. SLE illustrates type III because the injury follows complex deposition in vessels and glomeruli.

Key point! When a licensure question asks for the hypersensitivity mechanism of SLE, the expected answer is type III, immune complex deposition. Other type III examples—serum sickness and post-streptococcal glomerulonephritis—reinforce the same pattern of circulating complex deposition followed by complement-mediated inflammation [1].References (research sources)

- [1]Breaking immunological tolerance in systemic lupus erythematosus.Research articlePieterse E, van der Vlag J (2014) · DOI: 10.3389/fimmu.2014.00164

## 임상 시나리오

SLE and Type III HypersensitivityImmune complex deposition drives multisystem injury
In SLE, autoantibodies bind circulating self-antigens such as dsDNA and nucleosomes, forming soluble immune complexes. These deposit in vessels, glomeruli, joints, and skin, where they activate complement and recruit neutrophils, causing inflammation and tissue damage.

SLE is the classic type III hypersensitivity reaction. Other examples include serum sickness and post-streptococcal glomerulonephritis.

CautionSLE patients do produce autoantibodies such as anti-dsDNA, but the primary organ damage is from immune complex deposition, not direct antibody-mediated cytotoxicity. Do not confuse this with type II reactions like myasthenia gravis.

## 핵심 개념

- **Type III hypersensitivity** — Tissue injury caused by soluble antigen-antibody immune complexes that deposit in vessels and tissues, activate complement, and recruit neutrophils.
- **Immune complex** — A soluble aggregate of antigen bound to antibody that can deposit in vascular walls, glomeruli, joints, and skin.
- **Systemic lupus erythematosus** — A multisystem autoimmune disease characterized by autoantibodies to nuclear antigens such as dsDNA and nucleosomes, with immune complex–mediated organ damage.
- **Type II hypersensitivity** — Cytotoxic reaction in which IgG or IgM binds to cell surface or matrix antigens, as in myasthenia gravis.
- **Complement activation** — A cascade triggered by deposited immune complexes that promotes inflammation and neutrophil-mediated tissue injury.

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