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The upper airway is an important site of infection, but immune memory in the human upper airway is poorly understood, with implications for COVID-19 and many other human diseases1, 2, 3–4. Here we demonstrate that nasal and nasopharyngeal swabs can be used to obtain insights into these challenging problems, and define distinct immune cell populations, including antigen-specific memory B cells and T cells, in two adjacent anatomical sites in the upper airway. Upper airway immune cell populations seemed stable over time in healthy adults undergoing monthly swabs for more than 1 year, and prominent tissue resident memory T (TRM) cell and B (BRM) cell populations were defined. Unexpectedly, germinal centre cells were identified consistently in many nasopharyngeal swabs. In subjects with SARS-CoV-2 breakthrough infections, local virus-specific BRMcells, plasma cells and germinal centre B cells were identified, with evidence of local priming and an enrichment of IgA+memory B cells in upper airway compartments compared with blood. Local plasma cell populations were identified with transcriptional profiles of longevity. Local virus-specific memory CD4+TRMcells and CD8+TRMcells were identified, with diverse additional virus-specific T cells. Age-dependent upper airway immunological shifts were observed. These findings provide new understanding of immune memory at a principal mucosal barrier tissue in humans.

This article serves as one of four responses to Dana Logan's 2017 JAAR article entitled, "Lean Closet: Asceticism in Postindustrial Consumer Culture." It investigates the value of genealogical method for the field of American religious history and establishes both benefits and drawbacks to its application.

To identify the genetic cause of a syndrome causing cerebellar ataxia and eye movement abnormalities.

The article presents letters from readers of the journal on topics such as the William T. Hornaday Silver Medal, alfalfa chips, and Boy Scout popcorn.

IN the course of other investigations1in which tyrosine was injected intraperitoneally it was noted that the level of phenylalanine hydroxylase in the liver of rats was diminished to about one-third the normal value. Since tyrosine added in vitro does not inhibit this enzyme activity2, the results were taken as evidence of product inhibition of enzyme synthesis. It was reasoned that added dietary tyrosine would decrease the enzyme formation and therefore lower the amount of phenylalanine being oxidized to tyrosine; the excess phenylalanine would then be transaminated to phenylpyruvate. Other workers3had already shown that phenylalanine added to liver slices would also inhibit the oxidation of tyrosine to acetoacetate and fumarate. It seemed worth while therefore to feed various combinations of tyrosine and phenylalanine in order to evaluate metabolic alterations in the rat. Initial experiments with Commercial rat food plus 5 per cent L-tyrosine and 5 per cent DL-phenylalanine resulted in the death of newborn or suckling animals when this diet was fed to the pre-parturient and lactating mothers. The same diet caused death when fed to 21-day-old animals, although animals of the same age grew normally when fed 5 per cent of either amino-acid alone. Reduction of the levels to 2.5 per cent of each amino-acid (and in a later experiment to 3.75 per cent each) caused no difficulty since animals fed this diet gained weight at a rate comparable to that of rats on the commercial diet alone. The methods used for the amino-acid analyses and for enzyme assays have been previously listed1. The urinary and blood data are given in Table 1, and the enzymatic data concerned with phenylalanine and tyrosine metabolism are given in Table 2.