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Early infancy represents a critical window of immune system maturation during which transient dysregulation may result in atypical inflammatory or autoimmune-like phenotypes. Distinguishing such self-limited processes from true systemic autoimmune disease remains a major clinical challenge. We report an infant presenting with prominent cutaneous manifestations, markedly elevated inflammatory markers, hypocomplementemia, and broad high-titer autoantibody positivity including antinuclear, anti-dsDNA, extractable nuclear antigen, and antineutrophil cytoplasmic antibodies. Despite a laboratory profile strongly suggestive of systemic autoimmune disease, the patient remained clinically stable without evidence of organ involvement, including renal, neurological, or cardiopulmonary systems. Immunophenotyping demonstrated lymphocytosis with expansion of CD19+ B cells, while T-cell subsets and natural killer cells remained within expected ranges. Interferon signature analysis was negative, and whole-exome sequencing did not identify a causative monogenic disorder. All immunological abnormalities resolved spontaneously without immunosuppressive therapy. During follow-up, the patient developed transient neutropenia and atopic dermatitis, both with a self-limited course. This case highlights a transient systemic immune phenotype characterized by expansion of the CD19+ B-cell compartment, broad humoral immune activation and complement consumption in early infancy, followed by complete restoration of immune homeostasis. Recognition of such self-limited immune dysregulation is essential to avoid unnecessary immunosuppressive therapy and provides insight into mechanisms of immune tolerance during early human development.