ABSTRACT Impetigo is a common bacterial skin infection in children. Impetigo, primarily caused by Staphylococcus aureus and Group A Streptococcus (GAS). Along with changes in microbiological patterns and increasing antibiotic resistance, a better understanding of immunopathogenesis and measurable biological parameters is needed to assist in the diagnosis and evaluation of therapy in impetigo. This study aims to discusses innate and adaptive immune responses in impetigo and identifies quantitative biomarkers that have the potential to be used in clinical practice and research. The literature search was conducted using Google Scholar, ProQuest, PubMed, ScienceDirect, and the Wiley Online Library for publications from 2015 to 2025. The results of the synthesis show that activation of the innate immune response begins with pathogen recognition through PRRs on keratinocytes, followed by the release of proinflammatory cytokines, recruitment of neutrophils/macrophages, formation of NETs, and an increase in antimicrobial proteins. In S. aureus infection, colonization is influenced by adhesins (ClfB, SasG) and tissue damage is mediated by exfoliative toxins (ET), while immune evasion involves SpA, leukocidins, and inhibition of adaptive immune response formation. In GAS infection, virulence is influenced by M protein and various toxins/enzymes that can disrupt chemotaxis and neutrophil function. Potential quantitative biomarkers include leukocyte and neutrophil counts, CRP, IL-6, ROS, as well as more specific candidates such as ET-A/ET-B, PVL-SA, and SpyCEP. In the adaptive immune response, anti-SpA IgG3 has the potential to be a more specific marker for S. aureus infection, whereas ASO and ADB can support confirmation of GAS infection by considering age and geographic variation. The combination of general inflammatory biomarkers and more pathogen-specific biomarkers has the potential to accelerate diagnostic confirmation and assist in monitoring therapeutic response in impetigo. Keywords: Quantitative Biomarkers, Impetigo, Immunopathogenesis, Innate Immune Response, Adaptive Immune Response. ABSTRAK Impetigo merupakan infeksi bakteri kulit yang sering dijumpai pada anak. Penyebab utama impetigo adalah infeksi Staphylococcus aureus dan Group A Streptococcus (GAS). Seiring perubahan pola mikrobiologi dan meningkatnya resistensi antibiotik, diperlukan pemahaman imunopatogenesis yang lebih baik serta parameter biologis yang dapat diukur untuk membantu diagnosis dan evaluasi terapi pada impetigo. Penelitian ini bertujuan untuk membahas respons imun bawaan dan adaptif pada impetigo, serta mengidentifikasi biomarker kuantitatif yang berpotensi digunakan dalam praktik klinis maupun penelitian. Penelusuran literatur dilakukan pada Google Scholar, ProQuest, PubMed, ScienceDirect, dan Wiley online library untuk publikasi tahun 2015–2025. Hasil sintesis menunjukkan bahwa aktivasi respons imun bawaan dimulai dari pengenalan patogen melalui PRR pada keratinosit, diikuti pelepasan sitokin proinflamasi, rekrutmen neutrofil/makrofag, pembentukan NETs, serta peningkatan protein antimikroba. Pada S. aureus, kolonisasi dipengaruhi adhesin (ClfB, SasG) dan kerusakan jaringan dimediasi oleh toksin eksfoliatif (ET), sementara evasi imun melibatkan SpA, leukosidin, dan penghambatan pembentukan respons adaptif. Pada GAS, virulensi dipengaruhi protein M dan berbagai toksin/enzim yang dapat mengganggu kemotaksis serta fungsi neutrofil. Biomarker kuantitatif yang potensial meliputi jumlah leukosit dan neutrofil, CRP, IL-6, ROS, serta kandidat yang lebih spesifik seperti ET-A/ET-B, PVL-SA, dan SpyCEP. Pada respons adaptif, IgG3 anti-SpA berpotensi menjadi penanda yang lebih spesifik untuk infeksi S. aureus, sedangkan ASO dan ADB dapat mendukung konfirmasi infeksi GAS dengan mempertimbangkan variasi usia dan geografis. Kombinasi biomarker inflamasi umum dan biomarker yang lebih spesifik terhadap patogen berpotensi mempercepat diagnosis dan membantu pemantauan respons terapi pada impetigo. Kata Kunci: Biomarker Kuantitatif, Impetigo, Imunopatogenesis, Respons Imun Bawaan, Respons Imun Adaptif.
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