Purpose of review: Nonimmediate reactions to β-lactams include several clinical entities, from maculopapular rash to severe reactions such as Steven-Johnson syndrome. Toxic epidermal necrolysis and organ-specific reactions may also occur.
Recent findings: Progress has been made in understanding the role of the immunological system in nonimmediate reactions to β-lactams. Different T-cell subsets recognize β-lactams after haptenation of serum or cell proteins in the context of major histocompatibility complex. Studies using T-cell lines and clones have shown that a heterogeneous response is generated, with the expression of different cytokine profiles. Betalactams also act on dendritic cells, inducing changes that enable them to interact with naïve lymphocytes, becoming memory T cells. Tissue-activated CD4 and CD8 cells express perforin and other cytotoxic mediators that elicit the lesions. Studies on the clinical course of these entities indicate that cells migrate, establishing a recirculation with homing to the skin and back to the circulation. These cells thus participate not only in skin lesions but probably also in the repair process.
Summary: Understanding the immunological mechanisms involved in nonimmediate reactions to β-lactams has improved over the last few years, with better definition of the different T-cell subpopulations involved. Experimental studies and monitoring of the response support the implication of different cell subsets.