The past five or six years has seen a resurgence of interest in immunological memory. Areas in which important advances have been made of late or in which problems in understanding persist are covered here: (i) Selection of virgin B cells for entry into the peripheral pool. (ii) Expression of immunoglobulin isotypes and other markers on memory B cells. (iii) Development of memory B cells as a separate lineage from primary response B cells. (iv) Sites of production of memory B cells. (v) Signals that rescue mutating B cells in germinal centers, forming the basis of affinity selection, and programming further differentiation. (vi) The myriad markers of memory T cells, in particular CD45R isoforms. (vii) Selective migration pathways of memory T cells and its possible molecular basis. (viii) The lifespan of memory cells and factors that influence their long-term survival. The data accumulated during this period which have vastly increased our understanding of memory have at the same time highlighted unresolved problems that could block further progress in the field. The thorny question that we cannot at present answer is: How does a memory cell differ from an activated cell and, in the case of T cells, from an effector cell? The problem bears on the interpretation of any study that sets out to correlate memory phenotype with memory function. Immunologists may have donned an intellectual straitjacket in their search for the memory cell.

1. This paper confirms and extends several observations during the past 20 years that, despite many reports to the contrary, the rat is not unduly resistant to initial infection with tubercle bacilli provided they lodge in the lungs.2. The pattern of pathogenesis in the rat is probably closest to the now classical picture in the mouse, i.e. the response of a species with a low hypersensitivity potential. The pathology of the lesions agreed closely with the descriptions of Wessels (1941) and Kumashiro (1958b) resembling the mouse in most respects but, unlike the mouse, including the production of giant cells.3. When tested by footpad inoculation with 1/3·5 Old Tuberculin a positive reaction was demonstrated, commencing between 2 and 5 weeks after infection and persisting for several weeks. A fatal systemic reaction could often be induced with large doses of tuberculin given intraperitoneally.4. In a few cases loss of allergy was shown to be associated with a terminal anergic flare of the type observed previously in mice and guinea-pigs.

Insulin enhances Na(+)-K(+) pump activity in various noncardiac tissues. We examined whether insulin exposure in vitro regulates Na(+)-K(+) pump function in rabbit ventricular myocytes. Pump current (I(p)) was measured using the whole-cell patch-clamp technique at test potentials (V(m)s) from -100 to +60 mV. When the Na(+) concentration in the patch pipette ([Na](pip)) was 10 mM, insulin caused a V(m)-dependent increase in I(p). The increase was approximately 70% when V(m) was at near physiological diastolic potentials. This effect persisted after elimination of extracellular voltage-dependent steps and when K(+) and K(+)-congeners were excluded from the patch pipettes. When [Na](pip) was 80 mM, causing near-maximal pump stimulation, insulin had no effect, suggesting that it did not cause an increase in membrane pump density. Effects of tyrphostin A25, wortmannin, okadaic acid, or bisindolylmaleimide I in pipette solutions suggested that the insulin-induced increase in I(p) involved activation of tyrosine kinase, phosphatidylinositol 3-kinase, and protein phosphatase 1, whereas protein phosphatase 2A and protein kinase C were not involved.

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