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Memórias do Instituto Oswaldo Cruz
Fundação Oswaldo Cruz, Fiocruz
ISSN: 1678-8060 EISSN: 1678-8060
Vol. 92, Num. s2, 1997, pp. 173-182
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Mem Inst Oswaldo Cruz, Rio de Janeiro, Vol. 92 (Suppl.II), 1997, pp.
173-182
Human Eosinophil-Lymphocyte Interactions
Peter F Weller^+, Kaiser Lim
Department of Medicine, Beth Israel Deaconess Medical Center, DA-617
Harvard Medical School, 330 Brookline Ave., Boston, MA 02215, USA
^+Corresponding author. Fax:+1-617-277-6061. E-mail: pweller@bidmc.harvard.edu
Supported in part by grants (AI20241, AI22571) from the National Institutes
of Health and the MWV Leukocyte Research Fund.
Received 3 September 1997; Accepted 30 September 1997
Code Number:OC97183
Sizes of Files:
Text: 54.5K
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While the eosinophil's effector functions clearly can contribute to the
pathogenesis of allergic diseases, the evolutionary benefit to having
eosinophils as a distinct class of leukocytes is not clear, especially if
one must reconsider the nominally beneficial role of eosinophils in
parasite host defense. Eosinophils are equipped to respond to lymphocytes
and their cytokines (and not solely the eosinophil growth factor
cytokines), but the functional consequences of such eosinophil responses
need to be defined. Conversely, eosinophils, as antigen-presenting cells
(APCs) or sources of lymphocyte-active cytokines, may stimulate and effect
lymphocyte functioning. Eosinophils share with CD4^+ lymphocytes expression
of a number of receptors, including CD4 and IL-2R, and specific a4
integrins that may help in their common recruitment and activation.
Further, elucidation of the interactions between lymphocytes and
eosinophils will contribute to a broader understanding of the functioning
of eosinophils in "normal" ongoing immune responses and in allergic
disorders.
Key words: human eosinophil - lymphocite interactions - allergic
disorders
Knowledge of the functions and functioning of human eosinophils as
participants in immune responses remains incomplete. Normally in health,
the eosinophil is principally localized in submucosal tissue sites,
including the respiratory tract; but there is virtually no knowledge of how
eosinophils become localized in these submucosal sites or what roles
eosinophils play in normal, ongoing immune responses in these sites. Even
in diseases characterized by eosinophilia, helminthic infections and
allergic diseases, the functions of eosinophils are incompletely
understood.
Infections with helminthic parasites elicit eosinophilia, mediated by IL-5.
Based on in vitro studies demonstrating that eosinophils function as
helminthotoxic effector cells (Butterworth 1984), it has been hypothesized
that a major "beneficial" function of eosinophils is to participate in host
defense against helminthic parasites. This putatively beneficial role is
contrasted with some of the deleterious effects of eosinophils identified
for allergic diseases. Recent studies with anti-IL-5 antibody-treated,
helminth-infected mice, however, have questioned this role. In mice
infected with helminthic parasites, neutralizing anti-IL-5 antibody has
abrogated infection-induced blood, marrow and tissue eosinophilia. In these
anti-IL-5 (or anti-IL-4)-treated, eosinophil-deficient mice, intensities of
infections (both primary and secondary) have not been greater than in
eosinophilic mice (Sher et al. 1990, Herndon & Kayes 1992). Analogous
findings have been noted with parasitic infections in IL-5 knockout mice
(Foster et al. 1996) (PS Foster, unpublished). These findings argue against
a major role for eosinophils as helm-inthotoxic effector cells. While it is
possible that other host defense mechanisms against helminths are
sufficiently redundant that eosinophil ablation is not deleterious, these
findings with depletion of eosinophils raise the possibility that
eosinophils do not have a predominant helminthotoxic effector function in
host defense (Urban et al. 1992). Thus, the nominally beneficial function
of eosinophils in parasite host defense remains to be validated.
In allergic diseases, eosinophils are clearly participants and have
effector roles in promoting the pathogenesis of these diseases. Eosinophils
release lipid mediators, including leukotriene C4, platelet activating
factor and lipoxins (reviewed in Weller 1993), and contain four distinct
granule cationic proteins, major basic protein, eosinophil peroxidase,
eosinophil cationic protein and eosinophil derived neurotoxin, which may
cause dysfunction and destruction of other cells (reviewed in Gleich et al.
1992). These effector responses can be enhanced by exposures to specific
eosinophil-active cytokines, including the eosinophil growth factor
cytokines, GM-CSF, IL-3 and IL-5, which can be derived from T cells,
potentially of the Th2-like phenotype. It has long been recognized that
eosinophils from eosinophilic donors exhibit metabolic, morphologic, and
functional changes indicative that they have been "activated" in
vivo. Ongoing studies continue to provide evidence for this cytokine
"activation" of eosinophils. While the eosinophil-active growth factor
cytokines contribute to the process of eosinophil "activation", these
cytokines alone do not elicit all measures of eosin-ophil activation, such
as enhanced expression of FceRI (Gounni et al. 1994a) or CD40 (Ohkawara et
al. 1996) found on eosinophils from allergic subjects. Other cytokines or
tissue or extracellular matrix derived activating stimuli are likely to be
involved as well in augmenting specific functional capabilities of
eosinophils (Sedgwick et al. 1995).
Allergen-induced recruitment of eosinophils into lung tissues is correlated
with roles of CD4^+ T cells, presumably Th2 cells, and cytokines
released by such T cells (Iwamoto et al. 1993, Van Oosterhout et al. 1993,
Foster et al. 1996). In humans, IL-5 and to a lesser extent GM-CSF were the
predominant eosinophil survival-promoting cytokines in antigen-induced
pulmonary late-phase reactions (Ohnishi et al. 1993). The accumulation of
eosinophils in tissues, as in chronic asthma or following acute antigen
challenges in the lungs, correlates with measures of local T cell
activation (Wardlaw & Kay 1992). For instance, increases in activated T
lymphocytes, eosinophils, and cytokine mRNA expression for IL-5 and GM-CSF
have been documented in bronchial biopsies after allergen inhalation
challenge in atopic asthmatics (Bentley et al. 1993). Thus, there has been
an increasing recognition that eosinophil accumulation and enhanced
effector functions at tissue sites of allergic reactions may be intimately
related to lymphocyte activation, especially by nominally Th2-like
lymphocytes elaborating cytokines, including IL-5 and GM-CSF, that prolong
the viability and enhance the effector responses of mature eosinophils.
While there has been an increasing recognition of the roles of lymphocytes
in both the pathogenesis of allergic reactions and the regulation of
eosinophil involvement in such reactions, our central hypothesis, that
there exist collaborative interactions between lymphocytes and eosinophils
in respiratory tract tissue environments, is based on a number of
additional observations and considerations, as reviewed below. If
eosinophils function to help regulate lymphocyte responses to aeroallergens
encountered in the respiratory tract, such functions may be both
"beneficial" in normal mucosal immune responses and deleterious in
contributing to sustaining or propagating allergic reactions within the
airways.
Eosinophils As Airways Antigen-Presenting Cells For Lymphocytes
In hypothesizing roles for eosinophils as APCs, capable of eliciting
specific lymphocyte responses, a series of older observations on
eosinophils can be revisited and reinterpreted in light of our current
understanding of APCs.
Studies in the 1960's documented a remarkable capacity of eosinophils to
internalize administered antigen and to rapidly traffic to regional lymph
nodes. Primary injection of varied antigens (^3H-or fluorescently labeled)
into the foot pads of mice or guinea pigs was followed by antigen uptake
within eosinophils. Within one hr of antigen injection, eosinophils
containing the labeled antigens localized within regional lymph nodes (Litt
1964b, Roberts 1966). Uptake of antigen preferentially into eosinophils was
even greater when antibody to the antigen was present (Litt 1964a).
Moreover, repeated administration of antigen lead to even greater
localization of antigen-containing eosinophils in draining lymph nodes
(Litt 1963). Specific histologic stains to detect eosinophils in tissues
facilitated this recognition (Litt 1964a, b, Roberts 1966). While these
findings by themselves do not establish that eosinophils were serving as
APCs, these experiments do document roles for eosinophils in the very early
uptake of antigen, do indicate a role for antibody-facilitated uptake of
antigen by eosinophils, as antibody-facilitated uptake of antigen is now
recognized to enhance APC function, and do suggest that eosinophils exhibit
specific integrin-based or other mechanisms for preferential localization
within lymph nodes.
Eosinophils as Potential Antigen-Presenting Cells
If human eosinophils are to serve as effective APCs in vivo, several
conditions must be satisfied. Further, given the diversity of cells that
may function as professional and non-professional APCs, consideration must
be given to what specific capabilities eosinophils might have as distinct
APCs.
- For eosinophils to function as APCs, they must express Class II MHC
proteins. Blood eosinophils, from most normal and eosinophilic donors, lack
expression of Class II MHC proteins, even if these circulating eosinophils
otherwise exhibit evidence of phenotypic in vivo activation (Lucey
et al. 1989b). However, when mature, blood-derived human eosinophils are
cultured in vitro with specific cytokines, including IL-3, GM-CSF,
and IFN-g, these eosinophils are uniformly induced to synthesize and
express HLA-DR (Lucey et al. 1989b, Weller et al. 1993, Guida et al. 1994).
Thus, mature eosinophils have the capacity to express HLA-DR.
- Is there evidence that eosinophils in vivo express HLA-DR?
Notably, a number of observations document that airway eosinophils are
positive for HLA-DR expression. Eosinophils in the sputum of asthmatics
have been shown to express HLA-DR (Hansel et al. 1991). Airway, but not
blood, eosinophils in chronic eosinophilic pneumonia also have been
demonstrated to express HLA-DR (Beninati et al. 1993, Okubo et al. 1995,
Sakamoto et al. 1995b). In patients with asthma, even blood eosinophils
have been found to express greater HLA-DR than eosinophils from normals
(Sakamoto et al. 1995a). Moreover, comparisons of blood and bronchoalveolar
lavage eosinophils obtained 48 hr after segmental antigen (Sedgwick et al.
1992) or 4-6 hr after inhalational (Mengelers et al. 1994) challenges in
allergic subjects have demonstrated that HLA-DR was expressed on airway
eosinophils. Thus, the recruitment and activation of eosinophils into the
airways elicited by allergen challenge leads to the induction of HLA-DR
expression on the recruited airways eosinophils, which was not found on the
otherwise phenotypically activated blood eosinophils (Sedgwick et al. 1992,
Mengelers et al. 1994). Levels of Class II MHC protein expression need be
only low (210-340/cell) for a cell to function as an APC (Harding & Unanue
1990). Levels of HLA-DR fully sufficient for APC function are present on
eosinophils from the airways as recovered in the sputum or airway lavages
from allergic subjects.
- If eosinophils are to function as APCs, eosinophils must be able to
internalize protein, catabolize it and display the relevant peptides with
Class II MHC molecules. We have shown that eosinophils do function as
HLA-DR dependent, MHC-restricted antigen-presenting cells in stimulating
allogeneic T cell responses (Weller et al. 1993). Comparable findings have
been made with human T cell lines as responders (Hansel et al. 1992,
Wyss-Coray et al. 1993) and with murine eosinophils (Del Pozo et al. 1992,
Tamura et al. 1996).
- While presentation of antigen with MHC is necessary, full APC
function (i.e. "professional" APC) requires the presentation of
co-stimulatory signals by the APC. Accessory co-stimulatory molecules pair
with specific receptors on the T cell. The recognized molecular pairs
include B7-1 (CD80) or B7-2 (CD86) with CD28 or CTLA-4, ICAM-1 (CD54) or
ICAM-2 with LFA-1 (CD11a/CD18), LFA-3 (CD58) with CD2, and Class I and II
MHC molecules with CD8 and CD4, respectively. In addition, engagement of
CD40 on APCs can provide co-stimulation (Cella et al. 1996, Peng et al.
1996). We have demonstrated that eosinophils from allergic subjects express
CD40 (Lim et al. 1996b, Ohkawara et al. 1996) and that eosinophil CD40
provides co-stimulatory signals to CD3-activated T lymphocytes (Lim et al.
1996b). Other co-stimulatory molecules expressed by eosinophils include
ICAM-1 (CD54), which like HLA-DR is absent from circulating eosinophils,
but can be found on airway eosinophils and can be induced to be expressed
in vitro with specific cytokines (Czech et al. 1993, Hansel et al.
1992). Other eosinophil-derived chemokines or cytokines that can have
additional lymphocyte stimulatory activities are noted below. Thus,
eosinophils have the capacity to express Class II MHC, to present antigen
and to express relevant co-stimulatory molecules if such are induced in
vivo or in vitro.
Other Lymphocyte-Eosinophil Interactive Mechanisms
Eosinophils as sources of lymphocyte-active cytokines - Our studies
and those of others have documented that human eosinophils can synthesize
cytokines that include TGF-a (Wong et al. 1990, Elovic et al. 1994), TGF-b1
(Wong et al. 1991, Ohno et al. 1992, Elovic et al. 1994), TNF-a (Beil et
al. 1993, Costa et al. 1993), MIP-1a (Costa et al. 1993), IL-5 (Broide et
al. 1992; Desreumaux et al. 1992), GM-CSF (Kita et al. 1991, Moqbel et al.
1991, Ohno et al. 1991, Broide et al. 1992), IL-3 (Kita et al. 1991), IL-1a
(Weller et al. 1993), IL-6 (Hamid et al. 1992, Melani et al. 1993), IL-8
(Braun et al. 1993), IL-2 (Bosse et al. 1996, Levi-Schaffer et al. 1996),
IL-10 (Lamkhioued et al. 1995), IL-4 (Moqbel et al. 1995, Nonaka et al.
1995, Sabin et al. 1996), RANTES (Lim et al. 1995, 1996a; Ying et al. 1996)
and IL-16 (Lim et al. 1995, 1996a). We have shown that human eosinophils
elaborate lymphocyte chemoattractant activity that is largely mediated by
RANTES and IL-16 (Lim et al. 1995). Thus, human eosinophils are a source of
a cytokine (IL-16) and a chemokine (RANTES) specifically effecting the
functioning of CD4^+ lymphocytes (Cruikshank et al. 1994, 1996) and memory
T cells (Schall et al. 1990), respectively.
In addition, other eosinophil-derived cytokines, including IL-2 (Minami et
al. 1993), IL-4 (Aiello et al. 1990, Sabin et al. 1996), MIP-1a (Taub et
al. 1993), IL-1a (Ruppert & Peters 1991), IL-6 (Ruppert & Peters 1991) and
TGF-b1 (Ahuja et al. 1993, Lee & Rich 1993), have effects on lymphocytes.
Several beta chemokines, that can be elaborated by eosinophils, including
MIP-1a and RANTES, augment APC function and T cell responses and hence are
co-stimulatory (Taub et al. 1996). Thus, in addition to
eosinophil-lymphocyte cell-cell cognate interactions that may be active in
APC functioning of eosinophils, eosinophils can be sources of chemokines
and cytokines active on lymphocytes.
Eosinophil integrins - The expression of specific integrins by
eosinophils not only may contribute to their preferential recruitment into
sites of allergic diseases but also may help regulate their activation
within extravascular tissues (Resnick & Weller 1993) and their cell-cell
interactions (Munoz et al. 1996). We and others have shown that
eosinophils, and not neutrophils, express the a4b1 integrin VLA-4 (Bochner
et al. 1991, Dobrina et al. 1991, Weller et al. 1991). VLA-4 binds to
vascular cell adhesion molecule-1 (VCAM) and to domains within tissue
fibronectin (Elices et al. 1990). VLA-4, which is expressed in common on
eosinophils as well as lymphocytes and monocytes, but not neutrophils, can
mediate binding to VCAM, whose expression is inducible on endothelial cells
and can be demonstrated to be expressed in asthmatic bronchial vessels
(Ohkawara et al. 1995). By this means, preferential recruitment or
activation of eosinophils and mononuclear leukocytes might be expected.
Additionally, we have shown that eosinophils express another a4 integrin,
a4b7 (Erle et al. 1994, Wan et al. 1995). The expression of a4b7 on
eosinophils is intriguing given the role this integrin plays in binding to
the mucosal vascular addressin MAdCAM-1 (Berlin et al. 1993) and the
enhanced expression of a4b7 on a subsets of mucosal trophic CD4^+ memory T
lymphocytes (Schweighoffer et al. 1993, Rott et al. 1996). MAdCAM-1 is
known to be expressed on high endothelial venules of Peyer's patches and
mesenteric lymph nodes and sinus-lining cells in the spleen (Kraal et al.
1995). The common expression by eosinophils and some lymphocyte populations
of a4b7 may contribute to their co-localization within lymphoid tissues.
Moreover, the a4 integrins have been shown to be involved in cognate
cell-cell interactions (Munoz et al. 1996) including those specifically
between human lymphocytes and eosinophils (Mengelers et al. 1995).
Studies with blocking mAbs to the a4 component of both a4b1 and a4b7 have
demonstrated that such blockade can prevent eosinophil influx into
cutaneous or pulmonary sites of elicited allergic reactions (Weg et al.
1993, Pretolani et al. 1994). Moreover, blockade of a4 integrins can have
beneficial effects on allergic reactions even without inhibiting eosinophil
influx. In our collaborative studies, the administration of a blocking
anti-a4 mAb in allergic sheep was effective at preventing pulmonary late
phase reactions (Abraham et al. 1994). Anti-a4 mAb was effective when given
intravenously, before or after airway antigen challenge, and notably was
effective when given by aerosol within the airways (Abraham et al. 1994).
Despite its efficacy in blocking airway late phase reactions and bronchial
hyperreactivity, this anti-a4 mAb did not block influx of eosinophils into
the lung. The efficacy of the anti-a4 mAb administered directly within the
airways suggests that a4 integrin-mediated events with the airway lumen or
adjacent tissues were involved in activation of responses of a4 bearing
eosinophils and/or lymphocytes within the airways.
Other lymphocyte-mediated actions on eosinophils - Our studies have
identified mechanisms by which eosinophils are capable of responding to
lymphocyte-derived cytokines that do not enhance eosinophil effector
functions. Eosinophils express CD4 (Lucey et al. 1989a) and migrate in
response to the CD4-binding lymphokine, IL-16 (Rand et al. 1991a).
Eosinophils express high affinity IL-2 receptors and migrate in response to
IL-2 (Rand et al. 1991b). Eosinophils also express functional IL-4
receptors, and IL-4 can enhance eosinophil HLA-DR expression (Weller et al.
1993). None of these cytokines directly promotes "traditional" eosinophil
effector responses (e.g., degranulation); but their activities on
eosinophils further indicate that eosinophils have non-"traditional"
functions that can be modulated by lymphocyte-derived cytokines.
Potential specific roles for eosinophils as APCs - Diverse cells may
function as APCs, but different APCs have distinct roles in presenting
antigen as required for various immune responses, including initiating
primary immune responses, expanding "memory" T cell populations, and
potentially facilitating specific Th2 subset stimulation. These various
immune responses occur in different tissue sites, including spleen and
lymph nodes, and involve varied APCs, including dendritic cells, B cells
and macrophages, that have different functional capabilities and roles.
Specific roles for eosinophils as distinct APCs may be based on their
capacities to handle particulate antigens, their anatomic localizations and
subsequent tissue migrations, and their specific FcR-mediated abilities to
internalize antigens.
- Particulate antigen processing: antigen processing involves the
catabolism of antigens within APCs to produce immunogenic peptides that
bind to Class II MHC molecules. The requisite initial internalization of
antigens by APCs may occur via several mechanisms, including
receptor-mediated antigen uptake (e.g. mediated by surface immunoglobulin
on B cells), internalization of immune complexes by FcRs, nonspecific fluid
phase or absorptive uptake, and phagocytosis. While dendritic cells and B
cells very effectively present soluble protein antigens, they are unable to
handle particulate antigens (van Rooijen 1990). In the respiratory tract,
inhaled allergens are particulate (Platt-Mills 1992). Thus, while dendritic
cells are known to migrate from the airways (Havenith et al. 1993, Xia et
al. 1995), they would be ill-suited to process inhaled particulate
aeroallergens. Although dendritic cells in subepithelial tissues may be
effective APCs, it is unknown how particulate aeroallergens become
solubilized and traverse from the epithelium to these dendritic cells. The
principal cells recognized to ingest particulate antigens are phagocytic
macrophages (van Rooijen 1992); but alveolar macrophages are not effective
APCs and even antagonize APC function of dendritic cells (Gant et al. 1992,
Holt et al. 1993, Chelen et al. 1995, MacLean et al. 1996). Alternatively,
eosinophils would be well suited to handle particulate antigens, since
eosinophils are phagocytic, characteristically engage large, even
non-phago-cytosable multicellular targets and accumulate early at tissue
sites of particulate antigens (Kayes & Oaks 1978, Weller 1991).
- Eosinophil tissue localization and migration: the normal
localization of eosinophils within mucosal tissues of the respiratory, GI
and lower GU tracts would position them to encounter foreign antigens at
these mucosal surfaces. Moreover, in allergic airway diseases eosinophils
are characteristically found directly within the lumen and secretions of
airways. As noted above, these eosinophils express Class II MHC proteins
(Hansel et al. 1991) and could directly interact with inhaled particulate
allergens within the airways (Platt-Mills 1992).
- Antibody-mediated uptake of antigen: one especially effective
means of facilitating antigen uptake and processing by APCs involves
antibody targeting so that antigen is internalized complexed with antibody.
Both IgG- and IgE-dependent enhancement of APC antigen presentation have
been demonstrated. Antigen covalently coupled to anti-FcgRI, RII or RIII
receptor mAbs all enhanced antigen presentation by human
monocyte/macrophages (Gosselin et al. 1992), and high affinity FceRIs on
monocytes likewise have been shown to enhance allergen presentation (Maurer
et al. 1995). Complexing specific IgE antibody with antigen (Der p
II) facilitated CD23-dependent antigen presentation by EBV-B cells,
lowering 1000-fold the effective dose of antigen (van der Heijden et al.
1993). A role for IgE-mediated APC function in eliciting experimental
allergic airway eosinophilia and Th2 cytokine expression has been indicated
in anti-IgE treated and CD23 deficient mice (Coyle et al. 1996).
Human eosinophils express receptors for IgG (Hartnell et al. 1992), IgE
(Capron et al. 1992) and IgA (Abu-Ghazaleh et al. 1989, Monteiro et al.
1993). Human eosinophil IgE receptors include a variant of CD23 (Grangette
et al. 1989), the low affinity IgE receptor, and on some eosinophils,
especially those from patients with allergic diseases, the high affinity
FceRI receptor (Gounni et al. 1994b). Both CD23 and FceRI are detectable on
eosinophils in sites of allergic reactions (Tanaka et al. 1995, Humbert et
al. 1996), including the airways (Chihara et al. 1989, Humbert et al.
1996). In mucosal sites, eosinophils will be present with antibodies of all
three classes; and for inhaled allergens, IgG, IgE and IgA antibodies to
relevant antigens are measurable in mucosal secretions (Platts-Mills 1979,
Kitani et al. 1985, Desvaux et al. 1989). Interestingly, older studies of
eosinophils had demonstrated that eosinophils were very effective in the
uptake of antigen-antibody complexes (Sabesin 1963, Litt 1964a).
Thus, specific roles for the eosinophil as an APC may be related to its
capacity to process inhaled particulate allergens, its localization at and
migration from mucosal surfaces, and its expression of Fce, Fca and Fcg
receptors in sites where antibodies of these classes are directed against
relevant antigens. Thus, the hypothesis relevant to allergic asthma, in
which inhaled allergens, e.g. mite or cockroach, repetitively enter the
airways, is that Class II MHC expressing eosinophils, characteristically
present within the airways, have roles in processing antigen, transporting
it into tissues and presenting it to lymphocytes. Allergen-specific IgE and
eosinophil FceRs would facilitate this APC function of eosinophils.
Eosinophils as APCs may even bias lymphocyte responses to enhance Th2
responses (Wyss-Coray et al. 1993). This process of continued
antigen-presentation helps account for the chronicity of allergic
inflammation in response to inhaled allergens.
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