CELLULAR BASIS FOR IMMUNITY IN MALARIA 
243 
Bloom (1938a) that the free stem cells of 
the proposed polyphyletic theories, such as 
lymphoblasts, monoblasts, etc., do not exist 
as cell entities separate from lymphocytes. 
The free mesenchymal cells or lymphocytes 
are self-perpetuating by mitosis and un¬ 
questionably may arise from the fixed 
mesenchymal cells previously described. 
In malaria the free mesenchymal cells 
are of obvious importance as stem cells for 
the lymphoid and myeloid cells of the blood 
and connective tissue. In addition (see 
below) the lymphocyte is probably the 
single most important source of new macro¬ 
phages in malarial immunity. 
Systems of Cells in Immunity 
Modern concepts of systems of connec¬ 
tive tissue cells distributed over the body, 
which play a major part in immunity, have 
arisen fundamentally from studies on in¬ 
flammation. Among the early workers, 
great credit should be given Metchnikofl! 
(1892) for stressing the essential role of 
the connective tissue cells in inflammation 
and to Cohnheim (1867), Ziegler (1891), 
Marchand (1924), and Maximow (1927a, 
1927b) for studying the histogenesis of the 
local inflammatory reactions. Metchnikofl 
laid the basis for the modern concept of 
the immunological significance of fixed 
and mobile cells of the connective tissue by 
phagocytosis. His concept was physiologi¬ 
cal. He distinguished (1) microphages 
which are identical with heterophils and 
(2) macrophages as used in this chapter 
except that he included phagocytic glial 
cells of the brain. Furthermore, studies 
on vital staining and the storage of col¬ 
loidal dyes, chiefly by Renaut, Maximow, 
Goldman, Tschaschin, Kiyono and Aschoff 
have laid the basis for the modern concept 
of macrophages. Aschoff’s (1924) retic- 
ulo-endothelial system, as broadly defined 
and as generally used, consists of the 
macrophages as outlined in this discussion 
and is synonymous with the macrophage 
system of many recent authors. 
Particular mention should be made of 
the Gefasswandzellen of the Marchand- 
Herzog school (Marchand 1924). This sys¬ 
tem of cells includes not only endothelial 
cells-, but also pericytes and adventitial 
macrophages which are supposed to arise 
from the endothelium of developing ves¬ 
sels. Unfortunately, many authors have 
interpreted the Gefasswand to signify only 
endothelium and to consider, therefore, 
that true endothelium is phagocytic either 
in situ or after desquamation or migration. 
One of the frequent accompaniments of 
immunity in malaria and other infections 
is the local increase of cells of the macro¬ 
phage or reticulo-endothelial system. This 
hyperplasia is frequently assumed to be 
caused exclusively by a proliferation of the 
macrophages or elements of the reticulo¬ 
endothelial system. As will be shown later, 
such a proliferation is an admitted source 
of the new macrophages, but detailed 
studies on simian malaria by Taliaferro 
and Mulligan (1937) indicate that most of 
the new macrophages arise from lympho¬ 
cytes, with or without the intervention of 
a monocyte stage. In order to group to¬ 
gether under one term both macrophages 
and all macrophage precursors which de¬ 
velop homoplasticly from preexisting 
macrophages or heteroplasticly from agran- 
ulocytes (lymphocytes and monocytes), 
Taliaferro and Mulligan (1937) proposed 
the term, lymphoid-macrophage system. 
This term would include not only macro¬ 
phages and lymphocytes, but other mono¬ 
nuclear exudate cells ( i.e ., Maximow’s 
polyblasts) which form the cellular exu¬ 
date in inflammation and which are so 
prominent in the spleen in malaria (see 
below). 
(1) Phagocytic phases of malarial im¬ 
munity. Malarial immunity is chiefly con¬ 
cerned with parasiticidal effects. There is 
no complete or lasting inhibition of repro¬ 
duction of the parasites. As originally 
noted by Golgi (1888) in infections of P. 
vivax and P. malariae and as has been 
found subsequently in infections in both 
man and animals, the parasites formed by 
asexual reproduction show a high death 
rate from the beginning of the infection. 
At first this death of the parasites is a 
natural immunity and represents the un- 
